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As the most commonly diagnosed cancer in women, and the primary cause of cancer death in women globally, (1) breast cancer continues to be a significant public health issue. Although [...]

We synthesized the epidemiologic evidence on the associations between per- and polyfluoroalkyl substances (PFAS) exposure and breast cancer risk. Our systematic review and meta-analysis included 18 and 11 articles, respectively, covering studies up to February 2023. The summary relative risks (RRs) estimated by random-effects meta-analyses did not support an association between PFAS and overall breast cancer risk (eg, a natural log (ln)-unit increase in serum/plasma concentrations [ng/mL] for perfluorooctanoate [PFOA] RR = 0.95; 95% CI, 0.77-1.18; perfluorooctane sulfonate [PFOS] RR = 0.98; 95% CI, 0.87-1.11). However, when limiting to studies that assessed exposures prior to a breast cancer diagnosis, we observed a positive association with PFOA (a ln-unit increase, RR = 1.16; 95% CI, 0.96-1.40). We also observed some possible heterogeneous associations by tumor estrogen and progesterone receptor status among postmenopausal breast cancer cases. No meaningful changes were observed after excluding the studies with high risk of bias (Tier 3). Based on the evaluation tool developed by the National Toxicology Program, given the heterogeneity across studies and the variability in timing of exposure measurements, the epidemiologic evidence needed to determine the association between PFAS exposure and breast cancer remains inadequate. Our findings support the need for future studies with improved study designs to determine this association. [ABSTRACT FROM AUTHOR]

Introduction More than 73 million people in the United States live within 3 mi (5 km) of a Superfund site, (1) which can be sources of uncontrolled hazardous waste. These [...]

Background: Greenspace is hypothesized as being protective against cancer, whereas noise pollution and fine particulate matter (<2.5 μm in diameter, PM2.5) are both potential risk factors. Findings from recent studies of greenspace and PM2.5 with prostate cancer are not conclusive and the association between noise exposure and cancer has not been evaluated in a U.S. study. Methods: We assessed PM2.5, noise, and greenspace exposure using spatiotemporal models and satellite-based estimates at enrollment addresses for N = 43,184 male participants of the prospective Prostate, Lung, Colorectal, and Ovarian Cancer (PLCO) Screening Trial cohort (enrolled 1994-2001). We used Cox regression models adjusted for age, race and ethnicity, study center, family history of prostate cancer, and Area Deprivation Index to estimate associations between ambient PM2.5 (μg/m³), greenspace (index range from -1 to 1), and noise pollution (loudest 10% of total existing sound, decibels) and incident prostate cancer risk through December 2017. Results: A total of 6,327 cases of prostate cancer were diagnosed among male participants during follow-up. PM2.5 and noise exposures were moderately positively correlated (Spearman ρ = 0.46), and PM2.5 and greenspace were not correlated (ρ = 0.10); greenspace and noise were inversely correlated (ρ = -0.32). In single-pollutant and multipollutant models mutually adjusted for coexposures, we found no associations with prostate cancer risk. Conclusions: We did not find evidence that PM2.5, greenspace, and noise pollution were associated with prostate cancer risk in this large, geographically spread cohort. [ABSTRACT FROM AUTHOR]

Background Outdoor air pollution is a ubiquitous exposure that includes endocrine-disrupting and carcinogenic compounds that may contribute to the risk of hormone-sensitive outcomes such as uterine cancer. However, there is limited evidence about the relationship between outdoor air pollution and uterine cancer incidence. Methods We investigated the associations of residential exposure to particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5) and nitrogen dioxide (NO2) with uterine cancer among 33 417 Sister Study participants with an intact uterus at baseline (2003-2009). Annual average air pollutant concentrations were estimated at participants' geocoded primary residential addresses using validated spatiotemporal models. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals for the association between time-varying 12-month PM2.5 (µg/m3) and NO2 (parts per billion; ppb) averages and uterine cancer incidence. Results Over a median follow-up period of 9.8 years, 319 incident uterine cancer cases were identified. A 5-ppb increase in NO2 was associated with a 23% higher incidence of uterine cancer (hazard ratio = 1.23, 95% confidence interval = 1.04 to 1.46), especially among participants living in urban areas (hazard ratio = 1.53, 95% confidence interval = 1.13 to 2.07), but   PM2.5 was not associated with increased uterine cancer incidence. Conclusion In this large US cohort, NO2, a marker of vehicular traffic exposure, was associated with a higher incidence of uterine cancer. These findings expand the scope of health effects associated with air pollution, supporting the need for policy and other interventions designed to reduce air pollutant exposure. [ABSTRACT FROM AUTHOR]

Background Per- and polyfluoroalkyl substances (PFAS) are widespread and environmentally persistent chemicals with immunotoxic properties. Children are prenatally exposed through maternal transfer of PFAS to cord blood, but no studies have investigated the relationship with childhood leukemia. Methods We measured maternal serum levels of 19 PFAS in first-trimester samples collected in 1986-2010 and evaluated associations with acute lymphoblastic leukemia in full-term offspring (aged younger than 15 years) for 400 cases and 400 controls in the Finnish Maternity Cohort, matched on sample year, mother's age, gestational age, birth order, and child's sex. We analyzed continuous and categorical exposures, estimating odds ratios (ORs) and 95% confidence intervals (CIs) via conditional logistic regression adjusted for maternal smoking and correlated PFAS (ρ ≥ ±0.3). We also stratified by calendar period, mean diagnosis age, and the child's sex. Results N-methyl-perfluorooctane sulfonamidoacetic acid was associated with acute lymphoblastic leukemia in continuous models (per each doubling in levels: ORperlog2 = 1.22, 95% CI = 1.07 to 1.39), with a positive exposure-response across categories (OR>90th percentile = 2.52, 95% CI = 1.33 to 4.78; P trend = .01). Although we found no relationship with perfluorooctane sulfonic acid overall, an association was observed in samples collected in 1986-1995, when levels were highest (median = 17.9 µg/L; ORperlog2 = 4.01, 95% CI = 1.62 to 9.93). A positive association with perfluorononanoic acid was suggested among first births (P interaction = .06). The N-methyl-perfluorooctane sulfonamidoacetic acid association was mainly limited to children diagnosed before age 5 years (P interaction = .02). We found no consistent patterns of association with other PFAS or differences by sex. Conclusions These novel data offer evidence of a relationship between some PFAS and risk of the most common childhood cancer worldwide, including associations with the highest levels of perfluorooctanesulfonic acid and with a precursor, N-methyl-perfluorooctane sulfonamidoacetic acid. [ABSTRACT FROM AUTHOR]

Background Industrial facilities are not located uniformly across communities in the United States, but how the burden of exposure to carcinogenic air emissions may vary across population characteristics is unclear. We evaluated differences in carcinogenic industrial pollution among major sociodemographic groups in the United States and Puerto Rico. Methods We evaluated cross-sectional associations of population characteristics including race and ethnicity, educational attainment, and poverty at the census tract level with point-source industrial emissions of 21 known human carcinogens using regulatory data from the US Environmental Protection Agency. Odds ratios and 95% confidence intervals comparing the highest emissions (tertile or quintile) to the referent group (zero emissions [ie, nonexposed]) for all sociodemographic characteristics were estimated using multinomial, population density–adjusted logistic regression models. Results In 2018, approximately 7.4 million people lived in census tracts with nearly 12 million pounds of carcinogenic air releases. The odds of tracts having the greatest burden of benzene, 1,3-butadiene, ethylene oxide, formaldehyde, trichloroethylene, and nickel emissions compared with nonexposed were 10%-20% higher for African American populations, whereas White populations were up to 18% less likely to live in tracts with the highest emissions. Among Hispanic and Latino populations, odds were 16%-21% higher for benzene, 1,3-butadiene, and ethylene oxide. Populations experiencing poverty or with less than high school education were associated with up to 51% higher burden, irrespective of race and ethnicity. Conclusions Carcinogenic industrial emissions disproportionately impact African American and Hispanic and Latino populations and people with limited education or experiencing poverty thus representing a source of pollution that may contribute to observed cancer disparities. [ABSTRACT FROM AUTHOR]

Human exposure to per‐ and polyfluoroalkyl substances (PFAS) occurs globally through contaminated food, dust, and drinking water. Studies of PFAS and thyroid cancer have been limited. We conducted a nested case‐control study of prediagnostic serum levels of 19 PFAS and papillary thyroid cancer (400 cases, 400 controls) in the Finnish Maternity Cohort (pregnancies 1986‐2010; follow‐up through 2016), individually matched on sample year and age. We used conditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) for log2 transformed and categorical exposures, overall and stratified by calendar period, birth cohort, and median age at diagnosis. We adjusted for other PFAS with Spearman correlation rho = 0.3‐0.6. Seven PFAS, including perfluoroctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), N‐ethyl‐perfluorooctane sulfonamidoacetic acid (EtFOSAA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), and perfluorohexane sulfonic acid (PFHxS) were detected in >50% of women. These PFAS were not associated with risk of thyroid cancer, except for PFHxS, which was inversely associated (OR log2 = 0.82, 95% CI: 0.70‐0.97). We observed suggestive but imprecise increased risks associated with PFOA, PFOS, and EtFOSAA for those diagnosed at ages <40 years, whereas associations were null or inverse among those diagnosed at 40+ years (P‐interaction:.02,.08,.13, respectively). There was little evidence of other interactions. These results show no clear association between PFAS and papillary thyroid cancer risk. Future work would benefit from evaluation of these relationships among those with higher exposure levels and during periods of early development when the thyroid gland may be more susceptible to environmental harms. [ABSTRACT FROM AUTHOR]

Rationale: Particulate matter ≤2.5 μm in aerodynamic diameter (PM2.5) is an established cause of lung cancer, but the association with ultrafine particulate matter (UFP; aerodynamic diameter < 0.1 μm) is unclear. Objectives: To investigate the association between UFP and lung cancer overall and by histologic subtype. Methods: The Los Angeles Ultrafines Study includes 45,012 participants aged ≤50 years in southern California at enrollment (1995-1996) followed through 2017 for incident lung cancer (n = 1,770). We estimated historical residential ambient UFP number concentrations via land use regression and back extrapolation using PM2.5. In Cox proportional hazards models adjusted for smoking and other confounders, we estimated associations between 10-year lagged UFP (per 10,000 particles/cm³ and quartiles) and lung cancer overall and by major histologic subtype (adenocarcinoma, squamous cell carcinoma, and small cell carcinoma). We also evaluated relationships by smoking status, birth cohort, and historical duration at the residence. Measurements and Main Results: UFP was modestly associated with lung cancer risk overall (hazard ratio [HR], 1.03 [95% confidence interval (CI), 0.99-1.08]). For adenocarcinoma, we observed a positive trend among men; risk was increased in the highest exposure quartile versus the lowest (HR, 1.39 [95% CI, 1.05-1.85]; P for trend = 0.01) and was also increased in continuous models (HR per 10,000 particles/cm3, 1.09 [95% CI, 1.00-1.18]), but no increased risk was apparent among women (P for interaction = 0.03). Adenocarcinoma risk was elevated among men born between 1925 and 1930 (HR, 1.13 [95% CI, 1.02-1.26] per 10,000) but not for other birth cohorts, and was suggestive for men with ≤10 years of residential duration (HR, 1.11 [95% CI, 0.98-1.26]). We found no consistent associations for women or other histologic subtypes. Conclusions: UFP exposure was modestly associated with lung cancer overall, with stronger associations observed for adenocarcinoma of the lung. [ABSTRACT FROM AUTHOR]

Introduction Outdoor air pollution has been classified as a human carcinogen. (1) The evidence for breast cancer risk is accumulating although the specific constituents driving the association are not well [...]

BACKGROUND: Outdoor air pollution is a known lung carcinogen, but research investigating the association between particulate matter (PM) and gastrointestinal (GI) cancers is limited. OBJECTIVES: We sought to review the epidemiologic literature on outdoor PM and GI cancers and to put the body of studies into context regarding potential for bias and overall strength of evidence. METHODS: We conducted a systematic review and meta-analysis of epidemiologic studies that evaluated the association of fine PM [PM with an aerodynamic diameter of [less than or equal to]2.5 [micro]m (P[M.sub.2.5])] and P[M.sub.10] (aerodynamic diameter < 10 pm) with GI cancer incidence or mortality in adults. We searched five databases for original research published from 1980 to 2021 in English and summarized findings for studies employing a quantitative estimate of exposure overall and by specific GI cancer subtypes. We evaluated the risk of bias of individual studies and the overall quality and strength of the evidence according to the Navigation Guide methodology, which is tailored for environmental health research. RESULTS: Twenty studies met inclusion criteria and included participants from 14 countries; nearly all were of cohort design. All studies identified positive associations between PM exposure and risk of at least one GI cancer, although in 3 studies these relationships were not statistically significant. Three of 5 studies estimated associations with P[M.sub.10] and satisfied inclusion criteria for meta-analysis, but each assessed a different GI cancer and were therefore excluded. In the random-effects meta-analysis of 13 studies, P[M.sub.2.5] exposure was associated with an increased risk of GI cancer overall [risk ratio (RR) = 1.12; 95% CI: 1.01, 1.24]. The most robust associations were observed for liver cancer (RR = 1.31; 95% CI: 1.07, 1.56) and colorectal cancer (RR = 1.35; 95% CI: 1.08, 1.62), for which all studies identified an increased risk. We rated most studies with 'probably low' risk of bias and the overall body of evidence as 'moderate' quality with 'limited' evidence for this association. We based this determination on the generally positive, but inconsistently statistically significant, effect estimates reported across a small number of studies. CONCLUSION: We concluded there is some evidence of associations between P[M.sub.2.5] and GI cancers, with the strongest evidence for liver and colorectal cancers. Although there is biologic plausibility for these relationships, studies of any one cancer site were few and there remain only a small number overall. Studies in geographic areas with high GI cancer burden, evaluation of the impact of different PM exposure assessment approaches on observed associations, and investigation of cancer subtypes and specific chemical components of PM are important areas of interest for future research. https://doi.org/10.1289/EHP9620, Introduction Gastrointestinal (GI) cancers are a major cause of cancer burden and cancer death. Worldwide, there were an estimated 4.8 million new cases of GI cancers and 3.4 million GI [...]

A recent study published in the Journal of the National Cancer Institute examined the relationship between fine particulate matter (PM2.5), greenspace, and childhood cancer. While previous research has shown a link between PM2.5 and lung cancer in adults, there is limited evidence regarding childhood cancer. The study, conducted in Texas over a 16-year period, found associations between PM2.5 exposure and several types of childhood cancers, including acute lymphoblastic leukemia, retinoblastoma, ependymoma, non-Hodgkin lymphoma, thyroid carcinoma, and Hodgkin lymphoma. The study also explored the potential mitigating effects of greenspace on cancer risk, but the results were mixed. The findings highlight the complexity of environmental factors and their impact on childhood cancer risk, and further research is needed to better understand these relationships. [Extracted from the article]

Introduction Black women in the United States are more likely to develop breast cancer at a younger age and to be diagnosed with more aggressive subtypes and more advanced stage [...]

Background Fine particulate matter (PM2.5) has been inconsistently associated with breast cancer incidence, however, few studies have considered historic exposure when levels were higher. Methods Outdoor residential PM2.5 concentrations were estimated using a nationwide spatiotemporal model for women in the National Institutes of Health–AARP Diet and Health Study, a prospective cohort located in 6 states (California, Florida, Louisiana, New Jersey, North Carolina, and Pennsylvania) and 2 metropolitan areas (Atlanta, GA, and Detroit, MI) and enrolled in 1995-1996 (n = 196 905). Annual average PM2.5 concentrations were estimated for a 5-year historical period 10 years prior to enrollment (1980-1984). We used Cox regression to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between a 10 µg/m3 increase in PM2.5 and breast cancer incidence overall and by estrogen receptor status and catchment area. Results With follow-up of participants through 2017, a total of 15 870 breast cancer cases were identified. A 10 ug/m3 increase in PM2.5 was statistically significantly associated with overall breast cancer incidence (HR = 1.08, 95% CI = 1.02 to 1.13). The association was evident for estrogen receptor–positive (HR = 1.10, 95% CI = 1.04 to 1.17) but not estrogen receptor–negative tumors (HR = 0.97, 95% CI = 0.84 to 1.13; P heterogeneity = .3). Overall breast cancer hazard ratios were more than 1 across the catchment areas, ranging from a hazard ratio of 1.26 (95% CI = 0.96 to 1.64) for North Carolina to a hazard ratio of 1.04 (95% CI = 0.68 to 1.57) for Louisiana (P heterogeneity = .9). Conclusions In this large US cohort with historical air pollutant exposure estimates, PM2.5 was associated with risk of estrogen receptor–positive breast cancer. State-specific estimates were imprecise but suggest that future work should consider region-specific associations and the potential contribution of PM2.5 chemical constituency in modifying the observed association. [ABSTRACT FROM AUTHOR]