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BACKGROUND: The etiology of autism spectrum disorder is poorly understood. Few studies have investigated the link between endocrine-disrupting chemicals and autistic traits. We examined the relationship between gestational phthalates and autistic traits in 3- to 4-y-old Canadian children. We also investigated potential effect modification by sex and folic acid supplementation. METHODS: We enrolled 2,001 women >18 years of age during the first trimester of pregnancy between 2008 and 2011 from 10 cities in Canada. At 3–4 years of age, 610 children underwent neuropsychological assessments including the Social Responsiveness Scale–II (SRS-2) as a measure of autistic traits and social impairment. We measured 11 phthalate metabolites in maternal first trimester urine samples and assessed folic acid supplementation from reported intakes. We estimated covariate-adjusted differences in SRS-2 푇-scores with a doubling in phthalate concentrations in 510 children with complete data. RESULTS: Mean total SRS 푇-score was 45.3 (SD = 6.1). Children with higher gestational exposure to mono-n-butyl (MBP) and mono-3- carboxypropyl (MCPP) concentrations exhibited significantly higher total SRS 푇-scores, indicating greater overall social impairment, as well as higher scores on subdomains, indicating deficits in social cognition, social communication, social motivation, and restricted interests/repetitive behaviors. A doubling in MBP or MCPP concentrations was associated with 0.6 (95% CI: 0.1, 1.0) and 0.5 (95% CI: 0.1, 0.8) higher total SRS 푇-scores. Associations were consistently and significantly stronger in boys (ßMBP = 1.0; 95% CI: 0.4, 1.6; n = 252) compared with girls (ßMBP = 0.1; 95% CI: -0.6, 0.7; n = 258) and among children who had lower prenatal folic acid supplementation (<400 µg/d) (bMBP = 1:3; 95% CI: 0.4, 2.3; n = 59) compared with those who had adequate folic acid supplementation (=400 µg/d) (ßMBP = 0:4; 95% CI: -0:1, 0.8; n = 451). CONCLUSIONS: Higher gestational concentrations of some phthalate metabolites were associated with higher scores of autistic traits as measured by the SRS-2 in boys, but not girls; these small size effects were mitigated by first trimester-of-pregnancy folic acid supplementation. [ABSTRACT FROM AUTHOR]

Background: The role of environmental exposure to lead as a risk factor for chronic kidney disease (CKD) and its progression remains controversial, and most studies have been limited by a lack of direct glomerular filtration rate (GFR) measurement. Objective: We evaluated the association between lead exposure and GFR in children with CKD. Methods: In this cross-sectional study, we examined the association between blood lead levels (BLLs) and GFR measured by the plasma disappearance of iohexol among 391 participants in the Chronic Kidney Disease in Children (CKiD) prospective cohort study. Results: Median BLL and GFR were 1.2 µg/dL and 44.4 mL/min per 1.73 m2, respectively. The average percent change in GFR for each 1-µg/dL increase in BLL was −2.1 (95% CI: −6.0, 1.8). In analyses stratified by CKD diagnosis, the association between BLL and GFR was stronger among children with glomerular disease underlying CKD; in this group, each 1-µg/dL increase in BLL was associated with a −12.1 (95% CI: −22.2, −1.9) percent change in GFR. In analyses stratified by anemia status, each 1-µg/dL increase in BLL among those with and without anemia was associated with a −0.3 (95% CI: −7.2, 6.6) and −4.6 (95% CI: −8.9, −0.3) percent change in GFR, respectively. Conclusions: There was no significant association between BLL and directly measured GFR in this relatively large cohort of children with CKD, although associations were observed in some subgroups. Longitudinal analyses are needed to examine the temporal relationship between lead and GFR decline, and to further examine the impact of underlying cause of CKD and anemia/hemoglobin status among patients with CKD. [ABSTRACT FROM AUTHOR]

BACKGROUND: Prenatal bisphenol A (BPA) exposure has been associated with adverse neurodevelopment in epidemiological studies. However, prior studies had limited statistical power to examine sex-specific effects, and few examined child cognition. OBJECTIVES: We estimated the association between prenatal BPA exposure and child neurobehavior at 3 y of age in a prospective cohort of 812 mothers and their children. METHODS: We measured BPA concentration in urine samples collected at ∼12 wk gestation among women enrolled in a 10-city Canadian cohort study. At approximately 3 y of age, we assessed children's cognitive abilities with the Wechsler Primary and Preschool Scale of Intelligence™-III (WPPSI-III) and two scales of the Behavior Rating Inventory of Executive Function-Preschool (BRIEF-P). Parents reported children's behavior using the Behavior Assessment System for Children-2 (BASC-2) and the Social Responsiveness Scale™-2 (SRS-2). We estimated covariate-adjusted differences in neurobehavioral outcomes with a doubling in BPA concentration and sex-specific associations. RESULTS: BPA was not associated with WPPSI-III scores; child sex did not modify these associations. The association between BPA and BRIEF-P scores was modified by child sex (BPA×sex p-values≤0.03). For example, a doubling of BPA concentration was associated with 1-point (95% CI: 0.3, 1.7) poorer working memory in boys and 0.5-point (95% CI: -1.1, 0.1) better scores in girls. BPA was not associated with most BASC-2 scales; however, it was associated with more internalizing and somatizing behaviors in boys, but not in girls (BPA×sexp-values≤0.08). A doubling of BPA concentration was associated with poorer SRS-2 scores [β=0.3 ( 95% CI: 0, 0.7)]; this association was not modified by sex. CONCLUSION: Prenatal urinary BPA concentration was associated with some aspects of child behavior in this cohort, and some associations were stronger among boys. [ABSTRACT FROM AUTHOR]

Background: The role of traffic-related air pollution (TRAP) exposure in the development of allergic sensitization in children is unclear, and few birth cohort studies have incorporated spatiotemporal exposure assessment. Objectives: We aimed to examine the association between TRAP and atopy in 1-year-old children from an ongoing national birth cohort study in four Canadian cities. Methods: We identified 2,477 children of approximately 1 year of age with assessment of atopy for inhalant (Alternaria, Der p, Der f, cat, dog, cockroach) and food-related (milk, eggs, peanuts, soy) allergens. Exposure to nitrogen dioxide (NO2) was estimated from city-specific land use regression models accounting for residential mobility and temporal variability in ambient concentrations. We used mixed models to examine associations between atopy and exposure during pregnancy and the first year of life, including adjustment for covariates (maternal atopy, socioeconomic status, pets, mold, nutrition). We also conducted analyses stratified by time-location patterns, daycare attendance, and modeled home ventilation. Results: Following spatiotemporal adjustment, TRAP exposure after birth increased the risk for development of atopy to any allergens [adjusted odds ratio (aOR) per 10 μg/m3 NO2 = 1.16; 95% CI: 1.00, 1.41], but not during pregnancy (aOR = 1.02; 95% CI: 0.86, 1.22). This association was stronger among children not attending daycare (aOR = 1.61; 95% CI: 1.28, 2.01) compared with daycare attendees (aOR = 1.05; 95% CI: 0.81, 1.28). Trends to increased risk were also found for food (aOR = 1.17; 95% CI: 0.95, 1.47) and inhalant allergens (aOR = 1.28; 95% CI: 0.93, 1.76). Conclusion: Using refined exposure estimates that incorporated temporal variability and residential mobility, we found that traffic-related air pollution during the first year of life was associated with atopy. [ABSTRACT FROM AUTHOR]

BACKGROUND: Genetics may partially explain observed heterogeneity in associations between traffic-related air pollution and incident asthma. OBJECTIVE: Our aim was to investigate the impact of gene variants associated with oxidative stress and inflammation on associations between air pollution and incident childhood asthma. METHODS: Traffic-related air pollution, asthma, wheeze, gene variant, and potential confounder data were pooled across six birth cohorts. Parents reported physician-diagnosed asthma and wheeze from birth to 7-8 years of age (confirmed by pediatric allergist in two cohorts). Individual estimates of annual average air pollution [nitrogen dioxide (NO2), particulate matter ≤ 2.5 μm (PM2.5), PM2.5 absorbance, ozone] were assigned to each child's birth address using land use regression, atmospheric modeling, and ambient monitoring data. Effect modification by variants in GSTP1 (rs1138272/Ala114Val and rs1695/IIe105Val) and TNF (rs1800629/G-308A) was investigated. RESULTS: Data on asthma, wheeze, potential confounders, at least one SNP of interest, and NO2 were available for 5,115 children. GSTP1 rs1138272 and TNF rs1800629 SNPs were associated with asthma and wheeze, respectively. In relation to air pollution exposure, children with one or more GSTP1 rs1138272 minor allele were at increased risk of current asthma [odds ratio (OR) = 2.59; 95% CI: 1.43, 4.68 per 10 μg/m3 NO2] and ever asthma (OR = 1.64; 95% CI: 1.06, 2.53) compared with homozygous major allele carriers (OR = 0.95; 95% CI: 0.68, 1.32 for current and OR = 1.20; 95% CI: 0.98, 1.48 for ever asthma; Bonferroni-corrected interaction p = 0.04 and 0.01, respectively). Similarly, for GSTP1 rs1695, associations between NO2 and current and ever asthma had ORs of 1.43 (95% CI: 1.03, 1.98) and 1.36 (95% CI: 1.08, 1.70), respectively, for minor allele carriers compared with ORs of 0.82 (95% CI: 0.52, 1.32) and 1.12 (95% CI: 0.84, 1.49) for homozygous major allele carriers (Bonferroni-corrected interaction p-values 0.48 and 0.09). There were no clear differences by TNF genotype. CONCLUSIONS: Children carrying GSTP1 rs1138272 or rs1695 minor alleles may constitute a susceptible population at increased risk of asthma associated with air pollution. [ABSTRACT FROM AUTHOR]

BACKGROUND: Health agencies recommend that homes of heat-vulnerable occupants (e.g., older adults) be maintained below 24–28°C to prevent heat-related mortality and morbidity. However, there is limited experimental evidence to support these recommendations. OBJECTIVE: To aid in the development of evidence-based guidance on safe indoor temperatures for temperate continental climates, we evaluated surrogate physiological outcomes linked with heat-related mortality and morbidity in older adults during simulated indoor overheating METHODS: Sixteen older adults [six women; median age: 72 y, interquartile range (IQR): 70-73 y; body mass index: 24.6 (IQR: 22.1-27.0 kg/m²] from the Ottawa, Ontario, Canada, region (warm summer continental climate) completed four randomized, 8-h exposures to conditions experienced indoors during hot weather in continental climates (e.g., Ontario, Canada; 64 participant exposures). Ambient conditions simulated an air-conditioned environment (22°C; control), proposed indoor temperature upper limits (26°C), and temperatures experienced in homes without air-conditioning (31°C and 36°C). Core temperature (rectal) was monitored as the primary outcome; based on previous recommendations, between-condition differences >0.3C were considered clinically meaningful. RESULTS: Compared with 22°C, core temperature was elevated to a meaningful extent in 31°C [+0.7C; 95% confidence interval (CI): 0.5, 0.8] and 36°C (+0.9C; 95% CI: 0.8, 1.1), but not 26°C (+0.2C, 95% CI: 0.0, 0.3). Increasing ambient temperatures were also associated with elevated heart rate and reduced arterial blood pressure and heart rate variability at rest, as well as progressive impairments in cardiac and blood pressure responses to standing from supine. DISCUSSION: Core temperature and cardiovascular strain were not appreciably altered following 8-h exposure to 26°C but increased progressively in conditions above this threshold. These data support proposals for the establishment of a 26°C indoor temperature upper limit for protecting vulnerable occupants residing in temperate continental climates from indoor overheating. [ABSTRACT FROM AUTHOR]

BACKGROUND: Previous studies have identified the consumption of country foods (hunted/harvested foods from the land) as the primary exposure source of perfluoroalkyl acids (PFAA) in Arctic communities. However, identifying the specific foods associated with PFAA exposures is complicated due to correlation between country foods that are commonly consumed together. METHODS: We used venous blood sample data and food frequency questionnaire data from the Qanuilirpitaa? (“How are we now?”) 2017 (Q2017) survey of Inuit individuals ≥16 y of age residing in Nunavik (푛= 1,193). Adaptive elastic net, a machine learning technique, identified the most important food items for predicting PFAA biomarker levels while accounting for the correlation among the food items. We used generalized linear regression models to quantify the association between the most predictive food items and six plasma PFAA biomarker levels. The estimates were converted to percent changes in a specific PFAA biomarker level per standard deviation increase in the consumption of a food item. Models were also stratified by food type (market or country foods). RESULTS: Perfluorooctanesulfonic acid (PFOS), perfluorodecanoic acid (PFDA), and perfluoroundecanoic acid (PFUnDA) were associated with frequent consumption of beluga misirak (rendered fat) [14.6%; 95% confidence interval (CI): 10.3%, 18.9%; 14.6% (95% CI: 10.1%, 19.0%)], seal liver [9.3% (95% CI: 5.0%, 13.7%); 8.1% (95% CI: 3.5%, 12.6%)], and suuvalik (fish roe mixed with berries and fat) [6.0% (95% CI: 1.3%, 10.7%); 7.5% (95% CI: 2.7%, 12.3%)]. Beluga misirak was also associated with higher concentrations of perfluorohexanesulphonic acid (PFHxS) and perfluorononanoic acid (PFNA), albeit with lower percentage changes. PFHxS, perfluorooctanoic acid (PFOA), and PFNA followed some similar patterns, with higher levels associated with frequent consumption of ptarmigan [6.1% (95% CI: 3.2%, 9.0%); 5.1% (95% CI: 1.1%, 9.1%); 5.4% (95% CI: 1.8%, 9.0%)]. Among market foods, frequent consumption of processed meat and popcorn was consistently associated with lower PFAA exposure. CONCLUSIONS: Our study identifies specific food items contributing to environmental contaminant exposure in Indigenous or small communities relying on local subsistence foods using adaptive elastic net to prioritize responses from a complex food frequency questionnaire. In Nunavik, higher PFAA biomarker levels were primarily related to increased consumption of country foods, particularly beluga misirak, seal liver, suuvalik, and ptarmigan. Our results support policies regulating PFAA production and use to limit the contamination of Arctic species through long-range transport. [ABSTRACT FROM AUTHOR]

BACKGROUND: Toxic metals, such as lead (Pb), cadmium (Cd), arsenic (As), and mercury (Hg), may be associated with a higher risk of gestational hypertension and preeclampsia, whereas manganese (Mn) is an essential metal that may be protective. OBJECTIVES: We estimated the individual, independent, and joint associations of Pb, Cd, As, Hg, and Mn on the risk of developing gestational hypertension and preeclampsia in a cohort of Canadian women. METHODS: Metal concentrations were analyzed in first and third trimester maternal blood (푛=1,560). We measured blood pressure after 20 wk gestation to diagnose gestational hypertension, whereas proteinuria and other complications defined preeclampsia. We estimated individual and independent (adjusted for coexposure) relative risks (RRs) for each doubling of metal concentrations and examined interactions between toxic metals and Mn. We used quantile g-computation to estimate the joint effect of trimester-specific exposures. RESULTS: Each doubling of third trimester Pb (RR = 1.54; 95% CI: 1.06, 2.22) and first trimester blood As (RR = 1.25; 95% CI: 1.01, 1.58) was independently associated with a higher risk of developing preeclampsia. First trimester blood As (RR = 3.40; 95% CI: 1.40, 8.28) and Mn (RR = 0.63; 95% CI: 0.42, 0.94) concentrations were associated with a higher and lower risk, respectively, of developing gestational hypertension. Mn modified the association with As such that the deleterious association with As was stronger at lower concentrations of Mn. First trimester urinary dimethylarsinic acid concentrations were not associated with gestational hypertension (RR = 1.31; 95% CI: 0.60, 2.85) or preeclampsia (RR = 0.92; 95% CI: 0.68, 1.24). We did not observe overall joint effects for blood metals. DISCUSSION: Our results confirm that even low blood Pb concentrations are a risk factor for preeclampsia. Women with higher blood As concentrations combined with lower Mn in early pregnancy were more likely to develop gestational hypertension. These pregnancy complications impact maternal and neonatal health. Understanding the contribution of toxic metals and Mn is of public health importance. [ABSTRACT FROM AUTHOR]

BACKGROUND: Numerous epidemiological studies have documented the adverse health impact of long-term exposure to fine particulate matter [particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5)] on mortality even at relatively low levels. However, methodological challenges remain to consider potential regulatory intervention's complexity and provide actionable evidence on the predicted benefits of interventions. We propose the parametric g-computation as an alternative analytical approach to such challenges. METHOD: We applied the parametric g-computation to estimate the cumulative risks of nonaccidental death under different hypothetical intervention strategies targeting long-term exposure to PM2.5 in the Canadian Community Health Survey cohort from 2005 to 2015. On both relative and absolute scales, we explored the benefits of hypothetical intervention strategies compared with the natural course that a) set the simulated exposure value at each follow-up year to a threshold value if exposure was above the threshold (8.8 μg/m³, 7.04 μg/m³, 5 μg/m³, and 4 μg/m³), and b) reduced the simulated exposure value by a percentage (5% and 10%) at each follow-up year. We used the 3-y average PM2.5 concentration with 1-y lag at the postal code of respondents’ annual mailing addresses as their long-term exposure to PM2.5. We considered baseline and time-varying confounders, including demographics, behavior characteristics, income level, and neighborhood socioeconomic status. We also included the R syntax for reproducibility and replication. RESULTS: All hypothetical intervention strategies explored led to lower 11-y cumulative mortality risks than the estimated value under the natural course without intervention, with the smallest reduction of 0.20 per 1,000 participants (95% CI: 0.06, 0.34) under the threshold of 8:8 μg/m³, and the largest reduction of 3.40 per 1,000 participants (95% CI: -0.23, 7.03) under the relative reduction of 10% per interval. The reductions in cumulative risk, or numbers of deaths that would have been prevented if the intervention was employed instead of maintaining the status quo, increased over time but flattened toward the end of the follow-up period. Estimates among those ≥65 years of age were greater with a similar pattern. Our estimates were robust to different model specifications. DISCUSSION: We found evidence that any intervention further reducing the long-term exposure to PM2.5 would reduce the cumulative mortality risk, with greater benefits in the older population, even in a population already exposed to low levels of ambient PM2.5. The parametric g-computation used in this study provides flexibilities in simulating real-world interventions, accommodates time-varying exposure and confounders, and estimates adjusted survival curves with clearer interpretation and more information than a single hazard ratio, making it a valuable analytical alternative in air pollution epidemiological research. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exposure to fine particulate matter (PM2.5) during wildfire seasons has been associated with adverse health outcomes. Previous studies have focused on daily exposure, but PM2.5 levels in smoke events can vary considerably within 1 d. OBJECTIVES: We aimed to assess the immediate and lagged relationship between sub-daily exposure to PM2.5 and acute health outcomes during wildfire seasons in British Columbia. METHODS: We used a time-stratified case-crossover study design to evaluate the association between modeled hourly PM2.5 and ambulance dispatches during wildfire seasons from 2010 to 2015. Distributed lag nonlinear models were used to estimate the lag-specific and cumulative odds ratios (ORs) at lags from 1 to 48 h. We examined the relationship for all dispatches and dispatches related to respiratory, circulatory, and diabetic conditions, identified by codes for ambulance dispatch (AD), paramedic assessment (PA) or hospital diagnosis (HD). RESULTS: Increased respiratory health outcomes were observed within 1 h of exposure to a 10-μg/m³ increase in PM2.5. The 48-h cumulative OR [95% confidence interval (CI)] was 1.038 (1.009, 1.067) for the AD code Breathing Problems and 1.098 (1.013, 1.189) for PA code Asthma/COPD. The point estimates were elevated within 1 h for the PA code for Myocardial Infarction and HD codes for Ischemic Heart Disease, which had 24-h cumulative ORs of 1.104 (0.915, 1.331) and 1.069 (0.983, 1.162), respectively. The odds of Diabetic AD and PA codes increased over time to a cumulative 24-h OR of 1.075 (1.001, 1.153) and 1.104 (1.015, 1.202) respectively. CONCLUSIONS: We found increased PM2.5 during wildfire seasons was associated with some respiratory and cardiovascular outcomes within 1 h following exposure, and its association with diabetic outcomes increased over time. Cumulative effects were consistent with those reported elsewhere in the literature. These results warrant further investigation and may have implications for the appropriate time scale of public health actions. [ABSTRACT FROM AUTHOR]

BACKGROUND: Polybrominated diphenyl ethers (PBDEs) are flame retardants found in North American household products during the past four decades. These chemicals leach out in dust as products age, exposing individuals daily through inhalation and ingestion. Animal studies suggest that PBDEs disrupt sex hormones and adversely affect development of the reproductive system. OBJECTIVES: In the present study, we examined whether there is a link between maternal hair PBDE concentrations and the risk of cryptorchidism (undescended testes) in male infants; testis descent is known to be dependent on androgens. METHODS: Full-term male infants were recruited through clinics in Montreal, Toronto, and London, Canada. Boys with cryptorchidism at 3-18 months of age (n=137) were identified by pediatric urologists and surgeons; similar-aged controls (n=158) had no genitourinary abnormalities as assessed by pediatricians. Eight BDE congeners (BDE-28, -47, -99, -100, -153, -154, -183, -209) were measured by GC-MS (gas chromatography-mass spectrometry) in maternal hair samples collected at the time of recruitment. RESULTS: The ∑PBDE geometric mean for maternal hair was 45.35 pg/mg for controls and 50.27 pg/mg for cases; the concentrations of three BDEs (BDE-99, -100, and -154) were significantly higher in cases than controls in unadjusted models. In adjusted models, every 10-fold increase in the concentration of maternal hair BDE-99 [OR=2.53 (95% CI: 1.29, 4.95)] or BDE-100 [OR=2.45 (95% CI: 1.31, 4.56)] was associated with more than a doubling in the risk of cryptorchidism. BDE-154 [OR=1.88 (95% CI: 1.08, 3.28)] was also significant. CONCLUSIONS: Our results suggest that maternal exposure to BDE-99, -100, and -154 may be associated with abnormal migration of testes in the male fetus. This may be due to the anti-androgenic properties of the PBDEs. [ABSTRACT FROM AUTHOR]

Background: The impact of heat waves on mortality and health inequalities is well documented. Very few studies have assessed the effectiveness of heat action plans (HAPs) on health, and none has used quasi-experimental methods to estimate causal effects of such programs. Objectives: We developed a quasi-experimental method to estimate the causal effects associated with HAPs that allows the identification of heterogeneity across subpopulations, and to apply this method specifically to the case of the Montreal (Quebec, Canada) HAP. Methods: A difference-in-differences approach was undertaken using Montreal death registry data for the summers of 2000-2007 to assess the effectiveness of the Montreal HAP, implemented in 2004, on mortality. To study equity in the effect of HAP implementation, we assessed whether the program effects were heterogeneous across sex (male vs. female), age (≥ 65 years vs. < 65 years), and neighborhood education levels (first vs. third tertile). We conducted sensitivity analyses to assess the validity of the estimated causal effect of the HAP program. Results: We found evidence that the HAP contributed to reducing mortality on hot days, and that the mortality reduction attributable to the program was greater for elderly people and people living in low-education neighborhoods. Conclusion: These findings show promise for programs aimed at reducing the impact of extreme temperatures and health inequities. We propose a new quasi-experimental approach that can be easily applied to evaluate the impact of any program or intervention triggered when daily thresholds are reached. Citation: Benmarhnia T, Bailey Z, Kaiser D, Auger N, King N, Kaufman J. 2016. A difference-indifferences approach to assess the effect of a heat action plan on heat-related mortality, and differences in effectiveness according to sex, age, and socioeconomic status (Montreal, Quebec). Environ Health Perspect 124:1694-1699; http://dx.doi.org/10.1289/EHP203 [ABSTRACT FROM AUTHOR]

BACKGROUND: Although DDT [1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane] has been banned in many countries since the 1970s, it may still pose a risk to human respiratory health. In agriculture, DDT exposures have been associated with asthma and chronic bronchitis. However, little is known about the effect of DDT on lung function. OBJECTIVES: We examined DDT/DDE [1,1-bis-(4-chlorophenyl)-2,2-dichloroethene] concentrations in plasma and associations with lung function FVC (forced vital capacity), FEV1 (forced expiratory volume in 1 sec), FEV1/FVC ratio, and FEF25%-75% (forced expiratory flow between 25% and 75% of FVC). METHODS: We used data on 1,696 participants 20-79 years of age from the Canadian Health Measures Survey (CHMS) and conducted multiple regression analysis to estimate associations between plasma p,p '-DDT/DDE and lung function. RESULTS: Almost all participants (> 99.0%) had detectable concentrations of plasma p,p '-DDE, but only 10.0% had detectable p,p '-DDT. Participants with detectable p,p '-DDT had significantly lower mean FVC (difference = 311 mL; 95% CI: -492, -130; p = 0.003) and FEV1 (difference = 232 mL; 95% CI: -408,-55;p = 0.015) than those without. A 100-ng/g lipid increase in plasma p,p '-DDE was associated with an 18.8-mL decrease in mean FVC (95% CI: -29, -9) and an 11.8-mL decrease in mean FEV1 (95% CI: -21, -3). Neither exposure was associated with FEV1/FVC ratio or FEF25%-75%. CONCLUSIONS: DDT exposures, which may have occurred decades ago, were still detectable among Canadians. Plasma DDT and DDE were negatively associated with lung function parameters. Additional research on the potential effects of DDT use on lung function is warranted. [ABSTRACT FROM AUTHOR]

Background: Environmental determinants of appendicitis are poorly understood. Past work suggests that air pollution may increase the risk of appendicitis. Objectives: We investigated whether ambient ground-level ozone (O3) concentrations were associated with appendicitis and whether these associations varied between perforated and nonperforated appendicitis. Methods: We based this time-stratified case-crossover study on 35,811 patients hospitalized with appendicitis from 2004 to 2008 in 12 Canadian cities. Data from a national network of fixed-site monitors were used to calculate daily maximum O3 concentrations for each city. Conditional logistic regression was used to estimate city-specific odds ratios (ORs) relative to an interquartile range (IQR) increase in O3 adjusted for temperature and relative humidity. A random-effects meta-analysis was used to derive a pooled risk estimate. Stratified analyses were used to estimate associations separately for perforated and nonperforated appendicitis. Results: Overall, a 16-ppb increase in the 7-day cumulative average daily maximum O3 concentration was associated with all appendicitis cases across the 12 cities (pooled OR = 1.07; 95% CI: 1.02, 1.13). The association was stronger among patients presenting with perforated appendicitis for the 7-day average (pooled OR = 1.22; 95% CI: 1.09, 1.36) when compared with the corresponding estimate for nonperforated appendicitis [7-day average (pooled OR = 1.02, 95% CI: 0.95, 1.09)]. Heterogeneity was not statistically significant across cities for either perforated or nonperforated appendicitis (p > 0.20). Conclusions: Higher levels of ambient O3 exposure may increase the risk of perforated appendicitis. [ABSTRACT FROM AUTHOR]