Knowledge of the role in cancer etiology of environmental exposures as pesticides is a prerequisite for primary prevention. We review 63 epidemiological studies on exposure to pesticides and cancer risk in humans published from 2017 to 2021, with emphasis on new findings, methodological approaches, and gaps in the existing literature. While much of the recent evidence suggests causal relationships between pesticide exposure and cancer, the strongest evidence exists for acute myeloid leukemia (AML) and colorectal cancer (CRC), diseases in which the observed associations were consistent across several studies, including high‐quality prospective studies and those using biomarkers for exposure assessment, with some observing dose‐response relationships. Though high‐quality studies have been published since the IARC monograph on organophosphate insecticides in 2017, there are still gaps in the literature on carcinogenic evidence in humans for a large number of pesticides. To further knowledge, we suggest leveraging new techniques and methods to increase sensitivity and precision of exposure assessment, incorporate multi‐omics data, and investigate more thoroughly exposure to chemical mixtures. There is also a strong need for better and larger population‐based cohort studies that include younger and nonoccupationally exposed individuals, particularly during developmental periods of susceptibility. Though the existing evidence has limitations, as always in science, there is sufficient evidence to implement policies and regulatory action that limit pesticide exposure in humans and, hence, further prevent a significant burden of cancers.

PFAS (per-and polyfluoroalkyl substances) are a large class of synthetic chemicals widely used in consumer products and industrial processes. The scientific literature on PFAS has increased dramatically in the last decade. Many stakeholders, including regulators, scientists, non-governmental organizations, and concerned individuals could benefit from an efficient way to access the health and toxicological literature related to PFAS. To create a systematic evidence map of the available peer-reviewed health or toxicological research for 29 PFAS. A protocol for conducting this systematic evidence map was initially published on Zenodo (Pelch et al. 2019c), then peer reviewed and published in Environment International (Pelch et al. 2019d). PubMed database was searched through January 25, 2021. Studies were screened for inclusion and exclusion according to the Populations, Exposures, Comparators, and Outcomes (PECO) statement. Inclusion criteria were intentionally broad and included any human, animal, and/or in vitro study that investigated exposure to one of the 29 PFAS of interest and a human health or toxicological effect. Selected study details were extracted from included studies as described in the protocol. Study appraisal was not conducted. The included studies and extracted meta-data are freely available in the online, interactive systematic evidence map at https://pfastoxdatabase.org. Over 15,000 studies were retrieved from the PubMed literature searches. After manual screening, 1,067 studies were identified and included as investigating the health or toxicological effect of one or more PFAS of interest. There were 505 human, 385 animal, and 220 in vitro studies. Summary tables of the extracted data and overall observations are included in this report. The PFAS-Tox Database is a useful tool for searching, filtering, and identifying peer reviewed research on the health and toxicological effects of the included PFAS. In this summary of the evidence map we provide examples of data gaps and clusters revealed by the database, with the goal of helping direct future research efforts, facilitate systematic reviews (e.g. on immune effects, mixtures of PFAS, or effects of short chain PFAS), inform regulatory risk assessments, and improve opportunities for cross-disciplinary coordination. We also discuss how this tool supports scientists, regulatory agencies, and other individuals by increasing awareness and access to current evidence regarding the health effects associated with PFAS exposure.

Neighborhood conditions influence people’s health; sustaining healthy neighborhoods is a New York City (NYC) Health Department priority. Gentrification is characterized by rapid development in historically disinvested neighborhoods. The gentrification burden, including increased living expenses, and disrupted social networks, disproportionally impacts certain residents. To ultimately target health promotion interventions, we examined serious psychological distress time trends in gentrifying NYC neighborhoods to describe the association of gentrification and mental health overall and stratified by race and ethnicity. We categorized NYC neighborhoods as hypergentrifying, gentrifying, and not-gentrifying using a modified New York University Furman Center index. Neighborhoods with ≥100% rent growth were hypergentrifying; neighborhoods with greater than median and <100% rent growth were gentrifying; and neighborhoods with less than median rent growth were not-gentrifying. To temporally align neighborhood categorization closely with neighborhood-level measurement of serious psychological distress, data during 2000–2017 were used to classify neighborhood type. We calculated serious psychological distress prevalence among adult populations using data from 10 NYC Community Health Surveys during 2002–2015. Using joinpoint and survey-weighted logistic regression, we analyzed serious psychological distress prevalence time trends during 2002–2015 by gentrification level, stratified by race/ethnicity. Among 42 neighborhoods, 7 were hypergentrifying, 7 were gentrifying, and 28 were not gentrifying. In hypergentrifying neighborhoods, serious psychological distress prevalence decreased among White populations (8.1% to 2.3%, β = -0.77, P = 0.02) and was stable among Black (4.6% to 6.9%, β = -0.01, P = 0.95) and Latino populations (11.9% to 10.4%, β = -0.16, P = 0.31). As neighborhoods gentrified, different populations were affected differently. Serious psychological distress decreased among White populations in hypergentrifying neighborhoods, no similar reductions were observed among Black and Latino populations. This analysis highlights potential unequal mental health impacts that can be associated with gentrification-related neighborhood changes. Our findings will be used to target health promotion activities to strengthen community resilience and to ultimately guide urban development policies.

Prior research links prenatal exposure to organophosphate (OP) pesticides to adverse health outcomes via molecular mechanisms, such as oxidative stress, neurotransmitter disruption, and mitochondrial dysfunction. This study investigates such mechanisms by assessing the relationships between prenatal OP pesticide exposure and targeted urinary maternal metabolomic profiles using data from the New York University Children’s Health and Environment Study (NYU CHES) cohort (n = 890). Urine samples were collected at three time points during pregnancy (T1, T2, T3) and analyzed for six dialkyl phosphate (DAP) metabolites and a targeted set of 188 metabolites related to key biological functions. Associations between DAP concentrations and individual metabolites were estimated using linear and logistic regression models, with adjustment for potential confounders. Statistical analysis revealed significant associations between OP exposure and the studied maternal metabolomic profile, with the most associations observed during late pregnancy (T3). The most robust associations across all models and time points were observed for acylcarnitine profiles, which were consistently altered in association with OP exposure. This study identifies specific metabolic signatures associated with OP pesticide exposure during pregnancy, providing insights into potential mechanisms of toxicity and implications for maternal and child health. Additional research is needed to validate these findings and further understand the functional significance of the identified metabolic disturbances.