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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]

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]

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]

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 [...]