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Wildfires have become more frequent and intense due to climate change and outdoor wildfire fine particulate matter (PM2.5) concentrations differ from relatively smoothly varying total PM2.5. Thus, we introduced a conceptual model for computing long-term wildfire PM2.5 and assessed disproportionate exposures among marginalized communities. We used monitoring data and statistical techniques to characterize annual wildfire PM2.5 exposure based on intermittent and extreme daily wildfire PM2.5 concentrations in California census tracts (2006 to 2020). Metrics included: 1) weeks with wildfire PM2.5 < 5 μg/m3; 2) days with non-zero wildfire PM2.5; 3) mean wildfire PM2.5 during peak exposure week; 4) smoke waves (≥2 consecutive days with

BackgroundEvidence in the literature suggests that air pollution exposures experienced prenatally and early in life can be detrimental to normal lung development, however the specific timing of critical windows during development is not fully understood.ObjectivesWe evaluated air pollution exposures during the prenatal and early-life period in association with lung function at ages 6-9, in an effort to identify potentially influential windows of exposure for lung development.MethodsOur study population consisted of 222 children aged 6-9 from the Fresno-Clovis metro area in California with spirometry data collected between May 2015 and May 2017. We used distributed-lag non-linear models to flexibly model the exposure-lag-response for monthly average exposure to fine particulate matter (PM2.5) and ozone (O3) during the prenatal months and first three years of life in association with forced vital capacity (FVC), and forced expiratory volume in the first second (FEV1), adjusted for covariates.ResultsPM2.5 exposure during the prenatal period and the first 3-years of life was associated with lower FVC and FEV1 assessed at ages 6-9. Specifically, an increase from the 5th percentile of the observed monthly average exposure (7.55 μg/m3) to the median observed exposure (12.69 μg/m3) for the duration of the window was associated with 0.42 L lower FVC (95% confidence interval (CI): -0.82, -0.03) and 0.38 L lower FEV1 (95% CI: -0.75, -0.02). The shape of the lag-response indicated that the second half of pregnancy may be a particularly influential window of exposure. Associations for ozone were not as strong and typically CIs included the null.ConclusionsOur findings indicate that prenatal and early-life exposures to PM2.5 are associated with decreased lung function later in childhood. Exposures during the latter months of pregnancy may be especially influential.

Shift work is a common occupational exposure, however, few studies have examined aspects of shift work beyond night work and long hours, such as rotational patterns or weekend work, which may contribute to poor health through disruption of the bodys circadian rhythms. In this manuscript, we calculated the prevalence of working hour characteristics using algorithms for type (e.g., day), duration, intensity, rotational direction, and social aspects (e.g., weekend work) in a nationwide cohort of American manufacturing workers (N = 23,044) between 2003 and 2014. Distributions of working hour characteristics were examined by schedules (e.g., permanent day, day/night) and demographics, and were cross-classified in a matrix to examine co-occurrence. Approximately 55% of shifts may cause circadian rhythm disruption as they were non-day shifts or day shifts with a quick return or rotation, or were 13 h or longer. Older workers, female workers, and White workers worked permanent day shifts most often, while workers of color worked more day/night schedules. Night and evening shifts had more frequent shift rotations, quick returns, and longer hours than day shifts. Yet, day shifts, which are presumed to have little negative circadian impact, may cause circadian rhythm disruption as long hours, quick returns and rotations also occurred within day shifts.

In previous studies, investigators have reported increased risks of specific cancers associated with exposure to metalworking fluids (MWFs). In this report we broadly examine the incidence of 14 types of cancer, with a focus on digestive, respiratory, and hormonal cancers, in the United Auto Workers-General Motors (UAW-GM) cohort, a cohort of workers exposed to MWFs (1973-2015). The cohort included 39,132 workers followed for cancer incidence. Cox models yielded estimates of adjusted hazard ratios, with categorical variables for lagged cumulative exposure to 3 types of MWF (straight, soluble, and synthetic). We fitted penalized splines to examine the shape of the exposure-response relationships. There were 7,809 incident cancer cases of interest. Oil-based straight and soluble MWFs were each modestly associated with all cancers combined. Exposure-response patterns were consistent with prior reports from this cohort, and results for splined exposures generally reflected their categorically modeled counterparts. We found significantly increased incidence of stomach and kidney cancer with higher levels of straight MWF exposure and increased rectal and prostate cancer with increasing water-based synthetic MWF exposure. Only non-Hodgkin lymphoma and prostate cancer were associated with soluble MWF. All results for colon and lung cancers were null. Our results provide updated evidence for associations between MWF exposure and incidence of several types of cancer.

BackgroundDrought is an understudied driver of infectious disease dynamics. Amidst the ongoing southwestern North American megadrought, California (USA) is having the driest multi-decadal period since 800 CE, exacerbated by anthropogenic warming. In this study, we aimed to examine the influence of drought on coccidioidomycosis, an emerging infectious disease in southwestern USA.MethodsWe analysed California census tract-level surveillance data from 2000 to 2020 using generalised additive models and distributed monthly lags on precipitation and temperature. We then developed an ensemble prediction algorithm of incident cases of coccidioidomycosis per census tract to estimate the counterfactual incidence that would have occurred in the absence of drought.FindingsBetween April 1, 2000, and March 31, 2020, there were 81 448 reported cases of coccidioidomycosis throughout California. An estimated 1467 excess cases of coccidioidomycosis were observed in California in the 2 years following the drought that occurred between 2007 and 2009, and an excess 2649 drought-attributable cases of coccidioidomycosis were observed in the 2 years following the drought that occurred between 2012 and 2015. These increased numbers of cases more than offset the declines in cases that occurred during drought. An IQR increase in summer temperatures was associated with 2·02 (95% CI 1·84-2·22) times higher incidence in the following autumn (September to November), and an IQR increase in precipitation in the winter was associated with 1·45 (1·36-1·55) times higher incidence in the autumn. The effect of winter precipitation was 36% (25-48) stronger when preceded by two dry, rather than average, winters. Incidence in arid counties was most sensitive to precipitation fluctuations, while incidence in wetter counties was most sensitive to temperature.InterpretationIn California, multi-year cycles of dry conditions followed by a wet winter increases transmission of coccidioidomycosis, especially in historically wetter areas. With anticipated increasing frequency of drought in southwestern USA, continued expansion of coccidioidomycosis, along with more intense seasons, is expected. Our results motivate the need for heightened precautions against coccidioidomycosis in seasons that follow major droughts.FundingNational Institutes of Health.

BackgroundAlthough recent studies have identified important risk factors associated with incident carpal tunnel syndrome (CTS), risk factors associated with its severity have not been well explored.ObjectiveTo examine the associations between personal, workplace psychosocial and biomechanical factors and incident work disability among workers with CTS.MethodsBetween 2001 and 2010 five research groups conducted coordinated prospective studies of CTS and related work disability among US workers from various industries. Workers with prevalent or incident CTS (N=372) were followed for up to 6.4 years. Incident work disability was measured as: (1) change in work pace or work quality, (2) lost time or (3) job change following the development of CTS. Psychosocial factors were assessed by questionnaire. Biomechanical exposures were assessed by observation and measurements and included force, repetition, duty cycle and posture. HRs were estimated using Cox models.ResultsDisability incidence rates per 100 person-years were 33.2 for changes in work pace or quality, 16.3 for lost time and 20.0 for job change. There was a near doubling of risk for job change among those in the upper tertile of the Hand Activity Level Scale (HR 2.17; 95% CI 1.17 to 4.01), total repetition rate (HR 1.75; 95% CI 1.02 to 3.02), % time spent in all hand exertions (HR 2.20; 95% CI 1.21 to 4.01) and a sixfold increase for high job strain. Sensitivity analyses indicated attenuation due to inclusion of the prevalent CTS cases.ConclusionPersonal, biomechanical and psychosocial job factors predicted CTS-related disability. Results suggest that prevention of severe disability requires a reduction of both biomechanical and organisational work stressors.

Although air pollution is an important risk factor for stroke, few studies have considered the impact of workplace exposure to particulate matter (PM). We examined implications of exposure to PM composed of metalworking fluids (MWFs) for stroke mortality in the United Autoworkers-General Motors cohort. Cox proportional hazards models with age as the timescale were used to estimate the association of cumulative straight, soluble, and synthetic MWF exposure with stroke mortality, controlling for sex, race, plant, calendar year, and hire year. Among 38,553 autoworkers followed during 1941-1995, we identified 114 ischemic stroke deaths and 113 hemorrhagic stroke deaths. Overall stroke mortality risk was increased among workers in the middle exposure category for straight MWF (hazard ratio (HR) = 1.31, 95% confidence interval (CI): 0.87, 1.98) and workers in the highest exposure category for synthetic MWF (HR = 1.94, 95% CI: 1.13, 3.16) compared with workers who had no direct exposure. Ischemic stroke mortality risk was increased among workers in the highest exposure categories for straight MWF (HR = 1.45, 95% CI: 0.83, 2.52) and synthetic MWF (HR = 2.39, 95% CI: 1.39, 4.50). We observed no clear relationship between MWF exposure and hemorrhagic stroke mortality. Our results support a potentially important role for occupational PM exposures in stroke mortality and indicate the need for further studies of PM exposure and stroke in varied occupational settings.

BACKGROUND: Suicide, drug overdose, and alcohol-related liver disease (ALD) mortality have been rising in the United States. While suicide and overdose have received a great deal of attention, far less public health concern has focused on chronic ALD. To address this gap, we examine ALD mortality rates, by race, in a cohort of autoworkers to describe trends over the past 75 years, from the peak in automobile manufacturing employment through its decline. METHODS: Based on the United Autoworkers-General Motors (UAW-GM) cohort we estimated temporal trends in age-adjusted ALD mortality rates from 1941 through 2015 at three automobile manufacturing plants in Michigan. We compared these rates to county, state, and U.S. rates, directly standardized to the 2000 U.S. census, to assess the roles of race and employment on ALD mortality. RESULTS: The overall age-adjusted ALD mortality rate among 41,097 male autoworkers peaked at 46.1 per 100,000 in the 1970s, followed by a gradual decline and a recent rise. Rates were slightly higher for black than white men until early 2000s, when rates increased only for white men. ALD mortality rates in the study cohort tracked national, state, and county rates for white men until the most recent time period, but were lower throughout the study period for black men, especially in the 1970s and 1980s. CONCLUSIONS: Employment in automobile manufacturing may have offered some protection against death from ALD for black men, and loss of those manufacturing jobs may have impacted white men without a college degree more in recent decades.

BackgroundMetabolic syndrome increases the risk of cardiovascular disease in adults. Antecedents likely begin in childhood and whether childhood exposure to air pollution plays a contributory role is not well understood.ObjectivesTo assess whether children's exposure to air pollution is associated with markers of risk for metabolic syndrome and oxidative stress, a hypothesized mediator of air pollution-related health effects.MethodsWe studied 299 children (ages 6-8) living in the Fresno, CA area. At a study center visit, questionnaire and biomarker data were collected. Outcomes included hemoglobin A1c (HbA1c), urinary 8-isoprostane, systolic blood pressure (SBP), and BMI. Individual-level exposure estimates for a set of four pollutants that are constituents of traffic-related air pollution (TRAP) - the sum of 4-, 5-, and 6-ring polycyclic aromatic hydrocarbon compounds (PAH456), NO2, elemental carbon, and fine particulate matter (PM2.5) - were modeled at the primary residential location for 1-day lag, and 1-week, 1-month, 3-month, 6-month, and 1-year averages prior to each participant's visit date. Generalized additive models were used to estimate associations between each air pollutant exposure and outcome.ResultsThe study population was 53% male, 80% Latinx, 11% Black and largely low-income (6% were White and 3% were Asian/Pacific Islander). HbA1c percentage was associated with longer-term increases in TRAP; for example a 4.42 ng/m3 increase in 6-month average PAH456 was associated with a 0.07% increase (95% CI: 0.01, 0.14) and a 3.62 μg/m3 increase in 6-month average PM2.5 was associated with a 0.06% increase (95% CI: 0.01, 0.10). The influence of air pollutants on blood pressure was strongest at 3 months; for example, a 6.2 ppb increase in 3-month average NO2 was associated with a 9.4 mmHg increase in SBP (95% CI: 2.8, 15.9). TRAP concentrations were not significantly associated with anthropometric or adipokine measures. Short-term TRAP exposure averages were significantly associated with creatinine-adjusted urinary 8-isoprostane.DiscussionOur results suggest that both short- and longer-term estimated individual-level outdoor residential exposures to several traffic-related air pollutants, including ambient PAHs, are associated with biomarkers of risk for metabolic syndrome and oxidative stress in children.

BackgroundIn recent decades, suicide and fatal overdose rates have increased in the US, particularly for working-age adults with no college education. The coincident decline in manufacturing has limited stable employment options for this population. Erosion of the Michigan automobile industry provides a striking case study.MethodsWe used individual-level data from a retrospective cohort study of 26 804 autoworkers in the United Autoworkers-General Motors cohort, using employment records from 1970 to 1994 and mortality follow-up from 1970 to 2015. We estimated HRs for suicide or fatal overdose in relation to leaving work, measured as active or inactive employment status and age at worker exit.ResultsThere were 257 deaths due to either suicide (n=202) or overdose (n=55); all but 21 events occurred after leaving work. The hazard rate for suicide was 16.1 times higher for inactive versus active workers (95% CI 9.8 to 26.5). HRs for suicide were elevated for all younger age groups relative to those leaving work after age 55. Those 30-39 years old at exit had the highest HR for suicide, 1.9 (95% CI 1.2 to 3.0). When overdose was included, the rate increased by twofold for both 19- to 29-year-olds and 30- to 39-year-olds at exit. Risks remained elevated when follow-up was restricted to 5 years after exit.ConclusionsAutoworkers who left work had a higher risk of suicide or overdose than active employees. Those who left before retirement age had higher rates than those who left after, suggesting that leaving work early may increase the risk.

Objectives This report describes the extended follow-up (1941-2015) of a cohort of 38 549 automobile manufacturing workers with potential exposure to metalworking fluids (MWF). The outcomes of interest were mortality from cancers of the esophagus, stomach, intestine, rectum, bladder, liver, pancreas, larynx, lung, skin, prostate, brain, and female breast, as well as leukemia. This report includes 5472 deaths from cancer, more than ten times the numbers of deaths in our last summary report published 20 years ago. Methods Standardized mortality ratios were computed for the entire study period. Adjusted hazard ratios (HR) were estimated in Cox proportional hazard models with categorical variables for cumulative exposure to each type of MWF. Results Exposure-response patterns are consistent with prior mortality reports from this cohort. We found increased risk of skin and female breast cancer with straight fluids. For the first time, we found elevated risk of stomach cancer mortality. Overall, many of the exposure-response results did not suggest an association with MWF. Conclusions Mortality is a poor proxy for cancer diagnosis for treatable cancers and not the optimal outcome measure in etiological studies. Although the HR presented here handle bias from the healthy worker hire effect and left truncation, they do not handle bias from healthy worker survivor effect, which likely results in underestimates of the health impacts of MWF. Although this updated summary provides some information on the risk of cancer from MWF, targeted future analyses will help clarify associations.

BACKGROUND: Relatively few studies have examined the effects of layoffs on remaining workers, although the effects of layoffs and downsizing events may extend beyond those employees who lose their jobs. METHODS: We examined the effects of layoffs on mental healthcare utilisation and injury risk among workers at 30 US plants between 2003 and 2013. We defined layoffs as reductions in the hourly workforce of 20% or more at each plant. Using a difference-in-differences approach, we compared the change in outcomes during layoffs versus the same 3-month period 1 year previously, accounting for secular trends with control plants. RESULTS: Our study population included 15 502 workers and 7 layoff events between 2003 and 2013. Layoffs were associated with only minor decreases in injuries (-0.006, 95% CI -0.013 to 0.001). The probability of outpatient visits related to mental health increased by 1% during layoffs (0.010, 95% CI 0.003 to 0.017), and the probability of mental health-related prescriptions increased by 1.4% (0.014, 95% CI -0.0006 to 0.027). Among women, the increase in outpatient visits was more pronounced (0.017, 95% CI 0.003 to 0.031). Increased prescription utilisation appeared attributable primarily to opioid use (0.016, 95% CI 0.005 to 0.027). CONCLUSION: Our results indicate an association between layoffs and remaining workers mental health and safety, although changes mental healthcare utilisation may reflect both changes in underlying mental health and changes in care-seeking. Future research on concordance of service utilisation and underlying health may yield valuable insight into the experiences employed workers in the wake of layoffs.

Automotive technicians are commonly exposed to organic and chlorinated solvents, particularly through use of cleaning products. Mainly during the period 1989-2002, n-hexane was a component of some of these products. In other occupational contexts, n-hexane has been shown to be a cause of peripheral neuropathy. The purpose of the present study was to investigate whether previous exposures to low concentrations of n-hexane were a cause of persistent peripheral neuropathy in automotive technicians. Enrolled in the study were 830 San Francisco Bay Area automotive technicians. Each participant underwent a battery of tests to investigate peripheral nervous system impairment. Test results regressed against estimated hexane and total solvent exposures showed only limited evidence of association with solvent exposures. Exposures to both hexane and general solvents were well below their occupational exposure limits. Generally, our results provide reassurance about persistent peripheral neuropathic effects in automotive technicians who previously used hexane-containing automotive cleaning products. This may reflect repair processes, since the exposures occurred some years previous to the study. However, we cannot exclude the possibility that the absence of observed effect in this study may be attributable to low exposures, exposure misclassification and/or the healthy worker survivor effect.

ObjectiveOccupational dust exposure has been associated with accelerated lung function decline, which in turn is associated with overall morbidity and mortality. In the current study, we assess potential benefits on lung function of hypothetical interventions that would reduce occupational exposure to fine particulate matter (PM2.5) while adjusting for the healthy worker survivor effect.MethodsAnalyses were performed in a cohort of 6485 hourly male workers in an aluminium manufacturing company in the USA, followed between 1996 and 2013. We used the parametric g-formula to assess lung function decline over time under hypothetical interventions while also addressing time-varying confounding by underlying health status, using a composite risk score based on health insurance claims.ResultsA counterfactual scenario envisioning a limit on exposure equivalent to the 10th percentile of the observed exposure distribution of 0.05 mg/m3 was associated with an improvement in forced expiratory volume in one second (FEV1) equivalent to 37.6 mL (95% CI 13.6 to 61.6) after 10 years of follow-up when compared with the observed. Assuming a linear decrease and (from NHANES reference values), a 20 mL decrease per year for a 1.8 m-tall man as they age, this 37.6 mL FEV1 loss over 10 years associated with observed exposure would translate to approximately a 19% increase to the already expected loss per year from age alone.ConclusionsOur results indicate that occupational PM2.5 exposure in the aluminium industry accelerates lung function decline over age. Reduction in exposure may mitigate accelerated loss of lung function over time in the industry.

BackgroundStudies have reported associations between unconventional natural gas development (UNGD) and adverse birth outcomes. None have evaluated potential mediating mechanisms.ObjectivesTo evaluate associations between (1) UNGD and antenatal anxiety and depression and (2) antenatal anxiety and depression and preterm birth (

BackgroundTelomere length (TL) can serve as a potential biomarker for conditions associated with chronic oxidative stress and inflammation, such as asthma. Air pollution can induce oxidative stress. Understanding the relationship between TL, asthma, and air pollution is important for identifying risk factors contributing to unhealthy aging in children.ObjectivesWe sought to investigate associations between exposures to ambient air pollutants and TL in African American children and adolescents and to examine whether African ancestry, asthma status, and steroid medication use alter the association.MethodsLinear regression was used to examine associations between absolute telomere length (aTL) and estimated annual average residential ozone (O3) and fine particulate matter with a diameter of 2.5 μm or less (PM2.5) exposures in a cross-sectional analysis of 1072 children in an existing asthma case-control study. African ancestry, asthma status, and use of steroid medications were examined as effect modifiers.ResultsParticipants' aTLs were measured by using quantitative PCR. A 1-ppb and 1 μg/m3 increase in annual average exposure to O3 and PM2.5 were associated with a decrease in aTL of 37.1 kilo-base pair (kb; 95% CI, -66.7 to -7.4 kb) and 57.1 kb (95% CI, -118.1 to 3.9 kb), respectively. African ancestry and asthma were not effect modifiers; however, exposure to steroid medications modified the relationships between TL and pollutants. Past-year exposure to O3 and PM2.5 was associated with shorter TLs in patients without steroid use.ConclusionExposure to air pollution was associated with shorter TLs in nonasthmatic children and adolescents. This was not the case for asthmatic children as a group, but those receiving steroid medication had less shortening than those not using steroids. Reduced exposure to air pollution in childhood might help to preserve TL.

BackgroundMaternal smoking during pregnancy is a risk factor for chronic disease later in life and has been associated with variability of DNA methylation at specific cytosine-phosphate-guanine (CpG) loci. We assessed the role of DNA methylation as a potential mediator of adverse effects of in utero tobacco smoke exposures on asthma outcomes in Latino children from the US mainland and Puerto Rico.MethodsRelationships between self-reported exposure and DNA methylation at CpG loci previously reported to be associated with maternal smoking were assessed in a subsample consisting of 572 children aged 8-21 years (310 cases with asthma, 262 healthy controls), sampled from a larger asthma case-control study. Subsequently, we assessed associations between top loci and asthma-related outcomes, followed by mediation analysis for loci for which associations with outcomes were observed.ResultsSelf-reported maternal smoking was associated with a -1.5% (95% confidence interval (CI) = -2.4%, -0.6%) lower methylation at CpG locus cg05575921 on the AHRR gene; a 1% increase in DNA methylation at the same locus resulted in an odds ratio (OR) of 0.90 (95% CI = 0.83, 0.96) for the odds of asthma. The OR for the indirect effect of maternal smoking on asthma mediated through methylation at the cg05575921 locus was 1.18 (95% CI = 1.07, 1.68), compared to the OR for the total effect of exposure in the parent study of 1.48 (95% CI = 1.03, 2.11).ConclusionsOur findings suggest potential mediation by DNA methylation in the association between maternal smoking during pregnancy and asthma status.

Objectives Shift work, such as alternating day and nights, causes chronobiologic disruptions which may cause an increase in hypertension risk. However, the relative contributions of the components of shift work ‒ such as shift type (eg, night work) and rotations (ie, switching of shift times; day to night) ‒ on this association are not clear. To address this question, we constructed novel definitions of night work and rotational work and assessed their associations with risk of incident hypertension. Methods A cohort of 2151 workers at eight aluminum manufacturing facilities previously studied for cardiovascular disease was followed from 2003 through 2013 for incident hypertension, as defined by ICD-9 insurance claims codes. Detailed time-registry data was used to classify each worker's history of rotational and night work. The associations between recent rotational work and night work in the last 12 months and incident hypertension were estimated using adjusted Cox proportional hazards models. Results Elevated hazard ratios (HR) were observed for all levels of recent night work (>0-5, >5-50, >50-95, >95-100%) compared with non-night workers, and among all levels of rotational work (10-20, >20-30, and >30%) compared with those working

BackgroundIndustrial blue-collar workers face multiple work-related stressors, but evidence regarding the burden of mental illness among today's blue-collar men and women remains limited.MethodsIn this retrospective cohort study, we examined health and employment records for 37,183 blue- and white-collar workers employed by a single US aluminum manufacturer from 2003 to 2013. Using Cox proportional hazards regression, we modeled time to first episode of treated depression by gender and occupational class. Among cases, we modeled rates of depression-related service utilization with generalized gamma regression.ResultsCompared with their white-collar counterparts, blue-collar men were more likely to be treated for depression (hazard ratio [HR] = 1.3; 95% confidence interval [CI] = 1.1, 1.4) as were blue-collar women (HR = 1.4; 1.2, 1.6). Blue-collar women were most likely to be treated for depression as compared with white-collar men (HR = 3.2; 95% CI = 2.1, 5.0). However, blue-collar workers used depression-related services less frequently than their white-collar counterparts among both men (rate ratio = 0.91; 95% CI = 0.84, 0.98) and women (rate ratio = 0.82; 95% CI = 0.77, 0.88).ConclusionsBlue-collar women were more likely to be treated for depression than white-collar workers, and blue-collar women were most likely to be treated for depression compared with white-collar men. However, blue-collar men and women used depression-related healthcare services less frequently than white-collar workers. These findings underscore that blue-collar women may be uniquely susceptible to depression, and suggest that blue-collar workers may encounter barriers to care-seeking related mental illness other than their insurance status.

Diesel exhaust is a suggested risk factor for ischemic heart disease (IHD), but evidence from cohorts using quantitative exposure metrics is limited. We examined the impact of respirable elemental carbon (REC), a key surrogate for diesel exhaust, and respirable dust (RD) on IHD mortality, using data from the Diesel Exhaust in Miners Study in the United States. Using data from a cohort of male workers followed from 1948-1968 until 1997, we fitted Cox proportional hazards models to estimate hazard ratios for IHD mortality for cumulative and average intensity of exposure to REC and RD. Segmented linear regression models allowed for nonmonotonicity. Hazard ratios for cumulative and average REC exposure declined relative to the lowest exposure category before increasing to 0.79 and 1.25, respectively, in the highest category. Relative to the category containing the segmented regression change points, hazard ratios for the highest category were 1.69 and 1.54 for cumulative and average REC exposure, respectively. Hazard ratios for RD exposure increased across the full exposure range to 1.33 and 2.69 for cumulative and average RD exposure, respectively. Tests for trend were statistically significant for cumulative REC exposure (above the change point) and for average RD exposure. Our findings suggest excess risk of IHD mortality in relation to increased exposure to REC and RD.

Objectives In recent decades, risk of job loss in America after age 50 has been high, potentially causing significant stress during the period preceding retirement. Yet no study has quantified the burden of clinically relevant depressive symptoms attributable to job loss in this age group over this period or identified the most vulnerable populations. Methods Participants aged 50+ in the Health and Retirement Study (recruited 1992–2016) who were employed and scored <5 on the Center for Epidemiologic Studies-Depression 8-item scale (CESD-8) at baseline (N  = 18,571) were followed for depressive symptoms until they first had CESD-8 ≥5 or died, or through the 2018 survey. Parametric g-formula analyses examined the difference in cumulative risk of having CESD-8 ≥5 if there had been no involuntary job loss compared to the observed scenario, adjusting for sex, race/ethnicity, age, and dynamic measures of recent marriage end (divorce or widowhood), having a working spouse, assets/debt, and health changes. Results We estimated that risk of CESD-8 ≥5 would have been 1.1% (95% confidence interval [0.55, 1.37]) lower if no involuntary job loss had occurred; job loss accounted for 11% of the total burden among those who lost a job. Stronger associations were observed for women (1.2% [0.7, 1.8] vs men 0.5% [0.2, 1.1]), White respondents (1.0% [0.6, 1.5] vs Black respondents 0.5% [−0.1, 1.4]), and those in the lowest quartile of baseline assets (1.1% [0.4, 1.9] vs wealthiest quartile 0.5% [−0.4, 0.9]). Discussion Involuntary job loss is associated with high depressive symptom burden in older persons, suggesting that screening and intervention soon after job loss may help mitigate depression. [ABSTRACT FROM AUTHOR]

BackgroundSecondhand smoke (SHS) exposures have been linked to asthma-related outcomes but quantitative dose-responses using biomarkers of exposure have not been widely reported.ObjectivesAssess dose-response relationships between plasma cotinine-determined SHS exposure and asthma outcomes in minority children, a vulnerable population exposed to higher levels of SHS and under-represented in the literature.MethodsWe performed analyses in 1172 Latino and African-American children with asthma from the mainland USA and Puerto Rico. We used logistic regression to assess relationships of cotinine levels ≥0.05 ng/mL with asthma exacerbations (defined as asthma-related hospitalisations, emergency room visits or oral steroid prescription) in the previous year and asthma control. The shape of dose-response relationships was assessed using a continuous exposure variable in generalised additive logistic models with penalised splines.ResultsThe OR for experiencing asthma exacerbations in the previous year for cotinine levels ≥0.05 ng/mL, compared with

Exposure to silica has been linked to excess risk of lung cancer and nonmalignant respiratory disease mortality. In this study we estimated risk for both these outcomes in relation to occupational silica exposure as well as the reduction in risk that would result from hypothetical interventions on exposure in a cohort of exposed workers. Analyses were carried out using data from an all-male study population consisting of 2,342 California diatomaceous earth workers regularly exposed to crystalline silica and followed between 1942 and 2011. We estimated subdistribution risk for each event under the natural course and interventions of interest using the parametric g-formula to adjust for healthy-worker survivor bias. The risk ratio for lung cancer mortality, comparing an intervention in which a theoretical maximum exposure limit was set at 0.05 mg/m3 (the current US regulatory limit) with the observed exposure concentrations, was 0.86 (95% confidence interval: 0.63, 1.22). The corresponding risk ratio for nonmalignant respiratory disease mortality was 0.69 (95% confidence interval: 0.52, 0.93). Our findings suggest that risks from both outcomes would have been considerably lower if historical silica exposures in this cohort had not exceeded current regulatory limits.

Prolonged exposures can have complex relationships with health outcomes, as timing, duration, and intensity of exposure are all potentially relevant. Summary measures such as cumulative exposure or average intensity of exposure may not fully capture these relationships. We applied penalized and unpenalized distributed-lag nonlinear models (DLNMs) with flexible exposure-response and lag-response functions in order to examine the association between crystalline silica exposure and mortality from lung cancer and nonmalignant respiratory disease in a cohort study of 2,342 California diatomaceous earth workers followed during 1942-2011. We also assessed associations using simple measures of cumulative exposure assuming linear exposure-response and constant lag-response. Measures of association from DLNMs were generally higher than those from simpler models. Rate ratios from penalized DLNMs corresponding to average daily exposures of 0.4 mg/m3 during lag years 31-50 prior to the age of observed cases were 1.47 (95% confidence interval (CI): 0.92, 2.35) for lung cancer mortality and 1.80 (95% CI: 1.14, 2.85) for nonmalignant respiratory disease mortality. Rate ratios from the simpler models for the same exposure scenario were 1.15 (95% CI: 0.89, 1.48) and 1.23 (95% CI: 1.03, 1.46), respectively. Longitudinal cohort studies of prolonged exposures and chronic health outcomes should explore methods allowing for flexibility and nonlinearities in the exposure-lag-response.

Occupational exposure guidelines are ideally based on estimated effects of static interventions that assign constant exposure over a working lifetime. Static effects are difficult to estimate when follow-up extends beyond employment because their identifiability requires additional assumptions. Effects of dynamic interventions that assign exposure while at work, allowing subjects to leave and become unexposed thereafter, are more easily identifiable but result in different estimates. Given the practical implications of exposure limits, we explored the drivers of the differences between static and dynamic interventions in a simulation study where workers could terminate employment because of an intermediate adverse health event that functions as a time-varying confounder. The two effect estimates became more similar with increasing strength of the health event and outcome relationship and with increasing time between health event and employment termination. Estimates were most dissimilar when the intermediate health event occurred early in employment, providing an effective screening mechanism.

BACKGROUND:There is growing use of a job exposure matrix (JEM) to provide exposure estimates in studies of work-related musculoskeletal disorders; few studies have examined the validity of such estimates, nor did compare associations obtained with a JEM with those obtained using other exposures. OBJECTIVE:This study estimated upper extremity exposures using a JEM derived from a publicly available data set (Occupational Network, O*NET), and compared exposure-disease associations for incident carpal tunnel syndrome (CTS) with those obtained using observed physical exposure measures in a large prospective study. METHODS:2393 workers from several industries were followed for up to 2.8 years (5.5 person-years). Standard Occupational Classification (SOC) codes were assigned to the job at enrolment. SOC codes linked to physical exposures for forceful hand exertion and repetitive activities were extracted from O*NET. We used multivariable Cox proportional hazards regression models to describe exposure-disease associations for incident CTS for individually observed physical exposures and JEM exposures from O*NET. RESULTS:Both exposure methods found associations between incident CTS and exposures of force and repetition, with evidence of dose-response. Observed associations were similar across the two methods, with somewhat wider CIs for HRs calculated using the JEM method. CONCLUSION:Exposures estimated using a JEM provided similar exposure-disease associations for CTS when compared with associations obtained using the 'gold standard' method of individual observation. While JEMs have a number of limitations, in some studies they can provide useful exposure estimates in the absence of individual-level observed exposures.

Purpose of reviewWe offer an in-depth discussion of the time-varying confounding and selection bias mechanisms that give rise to the healthy worker survivor effect (HWSE).Recent findingsIn this update of an earlier review, we distinguish between the mechanisms collectively known as the HWSE and the statistical bias that can result. This discussion highlights the importance of identifying both the target parameter and the target population for any research question in occupational epidemiology. Target parameters can correspond to hypothetical workplace interventions; we explore whether these target parameters' true values reflect the etiologic effect of an exposure on an outcome or the potential impact of enforcing an exposure limit in a more realistic setting. If a cohort includes workers hired before the start of follow-up, HWSE mechanisms can limit the transportability of the estimates to other target populations. We summarize recent publications that applied g-methods to control for the HWSE, focusing on their target parameters, target populations, and hypothetical interventions.

ObjectiveThe main objective of this pilot study was to gather preliminary information about how telomere length (TL) varies in relation to exposure to polycyclic aromatic hydrocarbons (PAHs) in children living in a highly polluted city.MethodsWe conducted a cross-sectional study of children living in Fresno, California (n = 14). Subjects with and without asthma were selected based on their annual average PAH level in the 12-months prior to their blood draw. We measured relative telomere length from peripheral blood mononuclear cells (PBMC).ResultsWe found an inverse linear relationship between average PAH level and TL (R = 0.69), as well as between age and TL (R = 0.21). Asthmatics had shorter mean telomere length than non-asthmatics (TLasthmatic = 1.13, TLnon-asthmatic = 1.29).ConclusionsThese preliminary findings suggest that exposure to ambient PAH may play a role in telomere shortening.Become familiar with previous evidence suggesting that telomere length may be a biomarker of air pollution-induced cytotoxicity.Summarize the new findings on the association between polycyclic aromatic hydrocarbon (PAH) exposure and telomere length in adolescents, including those with asthma.Discuss the implications for recommendations and policies to mitigate the health and respiratory effects of traffic-related air pollution.

BackgroundBetween 2001 and 2010, six research groups conducted coordinated prospective studies of carpal tunnel syndrome (CTS) incidence among US workers from various industries to estimate exposure-response relationships.ObjectiveThis analysis examined the presence and magnitude of confounding between biomechanical and workplace psychosocial factors and incidence of dominant-hand CTS.Methods1605 participants, without CTS at enrolment, were followed for up to 3.5 years (2471 person-years). Demographic information, medical history and workplace psychosocial stress measures were collected at baseline. Individual workplace biomechanical exposures were collected for each task and combined across the workweek using time-weighted averaging (TWA). CTS case criteria were based on symptoms and results of electrophysiological testing. HRs were estimated with Cox proportional hazard models. Confounding was assessed using causal diagrams and an empirical criterion of 10% or greater change in effect estimate magnitude.ResultsThere were 109 incident CTS cases (IR=4.41/100 person-years; 6.7% cumulative incidence). The relationships between CTS and forceful repetition rate, % time forceful hand exertion and the Threshold Limit Value for Hand Activity Level (TLV-HAL) were slightly confounded by decision latitude with effect estimates being attenuated towards the null (10-14% change) after adjustment. The risk of CTS among participants reporting high job strain was attenuated towards the null by 14% after adjusting for the HAL Scale or the % time forceful hand exertions.ConclusionsAlthough attenuation of the relationships between CTS and some biomechanical and work psychosocial exposures was observed after adjusting for confounding, the magnitudes were small and confirmed biomechanical and work psychosocial exposures as independent risk factors for incident CTS.

ObjectivesMetalworking fluids (MWF), used to cool and lubricate metal in occupational settings, are linked to several cancers but data on kidney cancer are limited. We examine how MWF influence the rate of renal cell carcinoma (RCC) in a large prospective study.MethodsA cohort of Michigan autoworkers consisting of 33 421 individuals was followed from 1985 to 2009. The cohort was linked to the Michigan Cancer Registry to identify new cases of RCC. We analysed RCC in relation to cumulative exposure to each specific type of MWF (straight, soluble and synthetic) and all 3 types pooled into a single MWF variable, with a 15-year lag. Cox proportional hazards regression with splines were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), controlling for age, gender, race, calendar year, year hired, time since hire, plant and other MWF types.ResultsThere were 135 incident cases. A linear increase in the log-HR was observed for RCC with increasing cumulative exposure to each MWF type and total MWF exposure. At the mean of total MWF exposure (18.80 mg/m(3)-year), the estimated HR was 1.11 (95% CI 1.04 to 1.19).ConclusionsOur results provide evidence for a dose-dependent association between MWF exposure and RCC. The influence of components of oil-based and water-based MWF needs further examination.

ObjectivesLinks between arrhythmias and particulate matter exposures have been found among sensitive populations. We examined the relationship between personal particulate matter ≤2.5 µm aerodynamic diameter (PM2.5) exposures and ectopy in a panel study of healthy welders.MethodsSimultaneous ambulatory ECG and personal PM2.5 exposure monitoring with DustTrak Aerosol Monitor was performed on 72 males during work and non-work periods for 5-90 h (median 40 h). ECGs were summarised hourly for supraventricular ectopy (SVE) and ventricular ectopy (VE). PM2.5 exposures both work and non-work periods were averaged hourly with lags from 0 to 7 h. Generalised linear mixed-effects models with a random participant intercept were used to examine the relationship between PM2.5 exposure and the odds of SVE or VE. Sensitivity analyses were performed to assess whether relationships differed by work period and among current smokers.ResultsParticipants had a mean (SD) age of 38 (11) years and were monitored over 2993 person-hours. The number of hourly ectopic events was highly skewed with mean (SD) of 14 (69) VE and 1 (4) SVE. We found marginally significant increases in VE with PM2.5 exposures in the sixth and seventh hour lags, yet no association with SVE. For every 100 μg/m(3) increase in sixth hour lagged PM2.5, the adjusted OR (95% CI) for VE was 1.03 (1.00 to 1.05). Results persisted in work or non-work exposure periods and non-smokers had increased odds of VE associated with PM2.5 as compared with smokers.ConclusionsA small increase in the odds of VE with short-term PM2.5 exposure was observed among relatively healthy men with environmental and occupational exposures.

RationaleAdverse effects of exposures to ambient air pollution on lung function are well documented, but evidence in racial/ethnic minority children is lacking.ObjectivesTo assess the relationship between air pollution and lung function in minority children with asthma and possible modification by global genetic ancestry.MethodsThe study population consisted of 1,449 Latino and 519 African American children with asthma from five different geographical regions in the mainland United States and Puerto Rico. We examined five pollutants (particulate matter ≤10 μm and ≤2.5 μm in diameter, ozone, nitrogen dioxide, and sulfur dioxide), derived from participant residential history and ambient air monitoring data, and assessed over several time windows. We fit generalized additive models for associations between pollutant exposures and lung function parameters and tested for interaction terms between exposures and genetic ancestry.Measurements and main resultsA 5 μg/m(3) increase in average lifetime particulate matter less than or equal to 2.5 μm in diameter exposure was associated with a 7.7% decrease in FEV1 (95% confidence interval = -11.8 to -3.5%) in the overall study population. Global genetic ancestry did not appear to significantly modify these associations, but percent African ancestry was a significant predictor of lung function.ConclusionsEarly-life particulate exposures were associated with reduced lung function in Latino and African American children with asthma. This is the first study to report an association between exposure to particulates and reduced lung function in minority children in which racial/ethnic status was measured by ancestry-informative markers.

Occupational exposure to solvents, including n-hexane, has been associated with acquired color vision defects. Blue-yellow defects are most common and may be due to neurotoxicity or retinal damage. Acetone may potentiate the neurotoxicity of n-hexane. We present results on nonhexane solvent and hexane exposure and color vision from a cross-sectional study of 835 automotive repair workers in the San Francisco Bay Area, California (2007-2013). Cumulative exposure was estimated from self-reported work history, and color vision was assessed using the Lanthony desaturated D-15 panel test. Log-binomial regression was used to estimate prevalence ratios for color vision defects. Acquired color vision defects were present in 29% of participants, of which 70% were blue-yellow. Elevated prevalence ratios were found for nonhexane solvent exposure, with a maximum of 1.31 (95% confidence interval (CI): 0.86, 2.00) for blue-yellow. Among participants aged ≤50 years, the prevalence ratio for blue-yellow defects was 2.17 (95% CI: 1.03, 4.56) in the highest quartile of nonhexane solvent exposure and 1.62 (95% CI: 0.97, 2.72) in the highest category of exposure to hexane with acetone coexposure. Cumulative exposures to hexane and nonhexane solvents in the highest exposure categories were associated with elevated prevalence ratios for color vision defects in younger participants.

Little is known about the heart disease risks associated with occupational, rather than traffic-related, exposure to particulate matter with aerodynamic diameter of 2.5 µm or less (PM2.5). We examined long-term exposure to PM2.5 in cohorts of aluminum smelters and fabrication workers in the United States who were followed for incident ischemic heart disease from 1998 to 2012, and we addressed 2 forms of survivor bias. Left truncation bias was addressed by restricting analyses to the subcohort hired after the start of follow up. Healthy worker survivor bias, which is characterized by time-varying confounding that is affected by prior exposure, was documented only in the smelters and required the use of marginal structural Cox models. When comparing always-exposed participants above the 10th percentile of annual exposure with those below, the hazard ratios were 1.67 (95% confidence interval (CI): 1.11, 2.52) and 3.95 (95% CI: 0.87, 18.00) in the full and restricted subcohorts of smelter workers, respectively. In the fabrication stratum, hazard ratios based on conditional Cox models were 0.98 (95% CI: 0.94, 1.02) and 1.17 (95% CI: 1.00, 1.37) per 1 mg/m(3)-year in the full and restricted subcohorts, respectively. Long-term exposure to occupational PM2.5 was associated with a higher risk of ischemic heart disease among aluminum manufacturing workers, particularly in smelters, after adjustment for survivor bias.

BackgroundIf less healthy workers terminate employment earlier, thus accumulating less exposure, yet remain at greater risk of the health outcome, estimated health effects of cumulative exposure will be biased downward. If exposure also affects termination of employment, then the bias cannot be addressed using conventional methods. We examined these conditions as a prelude to a reanalysis of lung cancer mortality in the Diesel Exhaust in Miners Study.MethodsWe applied an accelerated failure time model to assess the effect of exposures to respirable elemental carbon (a surrogate for diesel) on time to termination of employment among nonmetal miners who ever worked underground (n = 8,307). We then applied the parametric g-formula to assess how possible interventions setting respirable elemental carbon exposure limits would have changed lifetime risk of lung cancer, adjusting for time-varying employment status.ResultsMedian time to termination was 36% shorter (95% confidence interval = 33%, 39%), per interquartile range width increase in respirable elemental carbon exposure. Lung cancer risk decreased with more stringent interventions, with a risk ratio of 0.8 (95% confidence interval = 0.5, 1.1) comparing a limit of ≤25 µg/m respirable elemental carbon to no intervention. The fraction of cases attributable to diesel exposure was 27% in this population.ConclusionsThe g-formula controlled for time-varying confounding by employment status, the signature of healthy worker survivor bias, which was also affected by diesel exposure. It also offers an alternative approach to risk assessment for estimating excess cumulative risk, and the impact of interventions based entirely on an observed population.

Ischemic heart disease (IHD) has been linked to exposures to airborne particles with an aerodynamic diameter

BackgroundCOPD is the third most frequent cause of death globally, with much of this burden attributable to household biomass smoke exposure in developing countries. As biomass smoke exposure is also associated with cardiovascular disease, lower respiratory infection, lung cancer, and cataracts, it presents an important target for public health intervention.MethodsLung function in Guatemalan women exposed to wood smoke from open fires was measured throughout the Randomized Exposure Study of Pollution Indoors and Respiratory Effects (RESPIRE) stove intervention trial and continued during the Chronic Respiratory Effects of Early Childhood Exposure to Respirable Particulate Matter (CRECER) cohort study. In RESPIRE, early stove households received a chimney woodstove at the beginning of the 18-month trial, and delayed stove households received a stove at trial completion. Personal exposure to wood smoke was assessed with exhaled breath carbon monoxide (CO) and personal CO tubes. Change in lung function between intervention groups and as a function of wood smoke exposure was assessed using random effects models.ResultsOf 306 women participating in both studies, acceptable spirometry was collected in 129 early stove and 136 delayed stove households (n = 265), with a mean follow-up of 5.6 years. Despite reduced wood smoke exposures in early stove households, there were no significant differences in any of the measured spirometric variables during the study period (FEV1, FVC, FEV1/FVC ratio, and annual change) after adjustment for confounding.ConclusionsIn these young Guatemalan women, there was no association between lung function and early randomization to a chimney stove or personal wood smoke exposure. Future stove intervention trials should incorporate cleaner stoves, longer follow-up, or potentially susceptible groups to identify meaningful differences in lung function.

BackgroundWe investigated the incidence of ischemic heart disease (IHD) in relation to accumulated exposure to particulate matter (PM) in a cohort of aluminum workers. We adjusted for time varying confounding characteristic of the healthy worker survivor effect, using a recently introduced method for the estimation of causal target parameters.MethodsApplying longitudinal targeted minimum loss-based estimation, we estimated the difference in marginal cumulative risk of IHD in the cohort comparing counterfactual outcomes if always exposed above to always exposed below a PM2.5 exposure cut-off. Analyses were stratified by sub-cohort employed in either smelters or fabrication facilities. We selected two exposure cut-offs a priori, at the median and 10th percentile in each sub-cohort.ResultsIn smelters, the estimated IHD risk difference after 15 years of accumulating PM2.5 exposure during follow-up was 2.9% (0.6%, 5.1%) using the 10th percentile cut-off of 0.10 mg/m. For fabrication workers, the difference was 2.5% (0.8%, 4.1%) at the 10th percentile of 0.06 mg/m. Using the median exposure cut-off, results were similar in direction but smaller in size. We present marginal incidence curves describing the cumulative risk of IHD over the course of follow-up for each sub-cohort under each intervention regimen.ConclusionsThe accumulation of exposure to PM2.5 appears to result in higher risks of IHD in both aluminum smelter and fabrication workers. This represents the first longitudinal application of targeted minimum loss-based estimation, a method for generating doubly robust semi-parametric efficient substitution estimators of causal parameters, in the fields of occupational and environmental epidemiology.

ObjectivesThe purpose of this study is to determine the trajectory of lung function change after exposure cessation to occupational organic dust exposure, and to identify factors that modify improvement.MethodsThe Shanghai Textile Worker Study is a longitudinal study of 447 cotton workers exposed to endotoxin-containing dust and 472 silk workers exposed to non-endotoxin-containing dust. Spirometry was performed at 5-year intervals. Air sampling was performed to estimate individual cumulative exposures. The effect of work cessation on forced expiratory volume in 1 s (FEV1) was modelled using generalised additive mixed effects models to identify the trajectory of FEV1 recovery. Linear mixed effects models incorporating interaction terms were used to identify modifiers of FEV1 recovery. Loss to follow-up was accounted for with inverse probability of censoring weights.Results74.2% of the original cohort still alive participated in 2011. Generalised additive mixed models identified a non-linear improvement in FEV1 for all workers after exposure cessation, with no plateau noted 25 years after retirement. Linear mixed effects models incorporating interaction terms identified prior endotoxin exposure (p=0.01) and male gender (p=0.002) as risk factors for impaired FEV1 improvement after exposure cessation. After adjusting for gender, smoking delayed the onset of FEV1 gain but did not affect the overall magnitude of change.ConclusionsLung function improvement after cessation of exposure to organic dust is sustained. Endotoxin exposure and male gender are risk factors for less FEV1 improvement.

UnlabelledA highly versatile nanoplatform that couples mesoporous silica nanoparticles (MSNs) with an aerosol technology to achieve direct nanoscale delivery to the respiratory tract is described. This novel method can deposit MSN nanoparticles throughout the entire respiratory tract, including nasal, tracheobronchial and pulmonary regions using a water-based aerosol. This delivery method was successfully tested in mice by inhalation. The MSN nanoparticles used have the potential for carrying and delivering therapeutic agents to highly specific target sites of the respiratory tract. The approach provides a critical foundation for developing therapeutic treatment protocols for a wide range of diseases where aerosol delivery to the respiratory system would be desirable.From the clinical editorDelivery of drugs via the respiratory tract is an attractive route of administration. In this article, the authors described the design of mesoporous silica nanoparticles which could act as carriers for drugs. The underlying efficacy was successfully tested in a mouse model. This drug-carrier inhalation nanotechnology should potentially be useful in human clinical setting in the future.

BackgroundRecently, the International Agency for Research on Cancer (IARC) Programme for the Evaluation of Carcinogenic Risks to Humans has been criticized for several of its evaluations, and also for the approach used to perform these evaluations. Some critics have claimed that failures of IARC Working Groups to recognize study weaknesses and biases of Working Group members have led to inappropriate classification of a number of agents as carcinogenic to humans.ObjectivesThe authors of this Commentary are scientists from various disciplines relevant to the identification and hazard evaluation of human carcinogens. We examined criticisms of the IARC classification process to determine the validity of these concerns. Here, we present the results of that examination, review the history of IARC evaluations, and describe how the IARC evaluations are performed.DiscussionWe concluded that these recent criticisms are unconvincing. The procedures employed by IARC to assemble Working Groups of scientists from the various disciplines and the techniques followed to review the literature and perform hazard assessment of various agents provide a balanced evaluation and an appropriate indication of the weight of the evidence. Some disagreement by individual scientists to some evaluations is not evidence of process failure. The review process has been modified over time and will undoubtedly be altered in the future to improve the process. Any process can in theory be improved, and we would support continued review and improvement of the IARC processes. This does not mean, however, that the current procedures are flawed.ConclusionsThe IARC Monographs have made, and continue to make, major contributions to the scientific underpinning for societal actions to improve the public's health.

BackgroundFew large epidemiologic studies have used rigorous case criteria, individual-level exposure measurements, and appropriate control for confounders to examine associations between workplace psychosocial and biomechanical factors and carpal tunnel syndrome (CTS).MethodsPooling data from five independent research studies, we assessed associations between prevalent CTS and personal, work psychosocial, and biomechanical factors while adjusting for confounders using multivariable logistic regression.ResultsPrevalent CTS was associated with personal factors of older age, obesity, female sex, medical conditions, previous distal upper extremity disorders, workplace measures of peak forceful hand activity, a composite measure of force and repetition (ACGIH Threshold Limit Value for Hand Activity Level), and hand vibration.ConclusionsIn this cross-sectional analysis of production and service workers, CTS prevalence was associated with workplace and biomechanical factors. The findings were similar to those from a prospective analysis of the same cohort with differences that may be due to recall bias and other factors.