Increasing PM2.5, NO2, NOx, and CO exposures were suggestively associated with increased CRC incidence, particularly among female and Latino participants and for left colon and rectal cancers.
Abstract
Growing evidence links air pollution to colorectal cancer (CRC) incidence. We examined this association within the large Multiethnic Cohort Study (MEC). Geocoded residential addresses for 98,675 California MEC participants were appended to ambient air pollution measures of PM2.5 (particulate matter [PM] with an aerodynamic diameter <2.5μm), PM10 (PM <10μm), nitrogen dioxide (NO2), nitrogen oxides (NOx), carbon monoxide (CO), and ozone (O3), generated from enrollment (1993-1996) to December 31, 2018. Multivariable-adjusted Cox proportional hazards models evaluated associations of time-varying air pollutants with CRC incidence (n=3,217 cases). We assessed heterogeneity in associations by demographics, tumor stage, and anatomical subsite. CRC incidence increased with PM2.5 exposure (per 10μg/m3; hazard ratio [HR]=1.13, 95% confidence interval [CI]=0.96-1.33), mainly among female (HR=1.29, 95% CI=1.03-1.62) but not among male participants (Pheterogeneity=0.08). CRC incidence also increased with NOx exposure among female (HR=1.22, 95% CI=1.01-1.48) but not male participants (Pheterogeneity=0.07). Increased incidence associated with PM2.5 (HR=1.36, 95% CI=1.05-1.76), NO2 (per 20 parts per billion [ppb]; HR=1.32, 95% CI=1.05-1.68) and CO (per 1000 ppb; HR=1.36, 95% CI=1.01-1.84) exposures were observed for left colon and rectal cancers combined, but not right colon cancers (Pheterogeneity by site=0.08, 0.06 and 0.13, respectively). Associations of PM2.5 and NO2 with rectal cancer incidence differed by population group (Pheterogeneity=0.04 and 0.03, respectively), and was mostly driven by positive associations among Latino participants. In summary, increasing PM2.5, NO2, NOx, and CO exposures were suggestively associated with increased CRC incidence, particularly among female and Latino participants and for left colon and rectal cancers.
The findings do not strongly support an association with invasive ovarian cancer, but suggest that air pollution, as indicated by NO₂ concentrations, may increase the risk of borderline tumours.
Lysandre Viau, S. Buteau, Anita Koushik· Cancer Epidemiology, Biomark...· 0 citations
Despite accumulating evidence linking air pollution to type 2 diabetes (T2D), the underlying mechanisms remain largely unexplored. We aimed to profile proteomic signatures associated with air pollution and examine their relationship to T2D. We conducted proteome-wide association studies on 2911 plasma proteins among 49,134 UK Biobank participants. Exposures to fine particulate matter (PM2.5), nitrogen dioxide (NO2), sulfur dioxide (SO2), and benzene were estimated based on residential addresses. Proteomic signatures and their corresponding scores for each air pollutant were identified using linear and elastic net regression models, comprising 368 proteins for PM2.5, 207 for NO2, 206 for SO2, and 236 for benzene. Cox proportional hazards regression models were subsequently used to examine the effect of air pollution and proteomic signature scores on the risk of incident T2D. In both the time-independent and time-dependent Cox models, all four air pollutants were significantly associated with higher T2D risk. In the time-dependent Cox models, the hazard ratios (HRs) and 95% confidence intervals (CIs) were 1.02 (1.00, 1.05) for PM2.5, 1.02 (1.01, 1.02) for NO2, 1.12 (1.06, 1.18) for SO2, and 1.88 (1.38, 2.57) for benzene, respectively. Higher proteomic signature scores of PM2.5, NO2, SO2, and benzene were also associated with an elevated risk of T2D, with HRs (95% CIs) of 1.05 (1.00, 1.09), 1.17 (1.12, 1.23), 1.11 (1.06, 1.16), and 1.11 (1.06, 1.16) for a per-standard-deviation increase, respectively. Moderate mediation effects of the proteomic signature scores were observed. Pathway analyses further implicated systemic inflammation as a potential underlying mechanism. Our findings suggested that air pollution might contribute to T2D risk through inflammation-related proteins, highlighting the potential of proteomics as a tool for precision public health. Building on this, our study also offered a framework to explore molecular pathways connecting modifiable risk factors to diseases.
Shenghao Yuan, Yongxuan Li, Yujia Bao et al.· Ecotoxicology and Environmen...· 0 citations
BACKGROUND
Air pollution is an established risk factor for cardiovascular and metabolic diseases, but evidence on chronic kidney diseases (CKD) remains limited.
OBJECTIVE
We aim to examine the association between long-term exposure to air pollutants and CKD incidence.
METHODS
We followed 24,581 female nurses from the Danish Nurse Cohort, recruited in 1993 or 1999, for their first-ever hospital contact with a primary or secondary CKD diagnosis until 2018. We estimated annual mean levels of particulate matter with a diameter < 2.5 µm (PM2.5) and 10 µm (PM10), nitrogen dioxide (NO2), and black carbon (BC) at nurses' residential addresses using the DEHM/UBM/AirGIS modeling system. We used Cox regression models to examine the association of 14-year running means of air pollutants with CKD incidence and to explore the effect modification of this association by lifestyles.
RESULTS
Over 521,211 person-years of follow-up, 429 nurses developed CKD. We found positive associations of modest magnitude between long-term exposure to air pollutants and CKD, with hazard ratios (95% confidence intervals) per interquartile range: 1.18 (0.93-1.50) per 2.86 µg/m3 for PM2.5, 1.14 (0.93-1.40) per 3.33 µg/m3 for PM10, 1.13 (0.99-1.28) per 8.09 µg/m3 for NO2, and 1.09 (1.00-1.20) per 0.34 µg/m3 for BC. The associations between long-term exposure to NO2 and CKD incidence were greater in never smokers than in ever-smokers. Associations with NO2 and BC remained unchanged in two-pollutant models, whereas those with PM10 and PM2.5 attenuated.
SIGNIFICANCE
Our study adds important new findings to the growing evidence suggesting that air pollution may be associated with CKD incidence.
IMPACT STATEMENT
This study provides longitudinal evidence that long-term exposure to ambient air pollution contributes to chronic kidney disease (CKD) incidence, even in a relatively healthy occupational cohort and at comparatively low pollution levels. Although effect sizes were modest, consistent positive associations, particularly for NO2 and black carbon, highlight traffic-related pollution as a potential renal risk factor. Stronger associations among never-smokers suggest that environmental exposures may independently influence kidney health. These findings reinforce the need to integrate air pollution into CKD risk assessment and prevention strategies. Strengthening air quality policies and reducing long-term residential exposure could help lower CKD burden and protect kidney health at the population level.
Gonzalo Hevia-Ramos, Jiawei Zhang, Stephane Tuffier et al.· Journal of Exposure Science...· 0 citations
Air pollution remains a major public health concern, particularly in large metropolitan areas. This study aimed to evaluate the short-term association between ambient air pollution levels and non-accidental mortality in Istanbul between 2013 and 2019. In this ecological time-series study, daily mortality data were analyzed using quasi-Poisson regression models incorporating distributed lag non-linear models (DLNM) to estimate exposure-response relationships. Citywide daily mean concentrations of major air pollutants were derived from all eligible monitoring stations. Effect estimates were expressed as relative risks (RRs) with 95% confidence intervals (CIs) per 10 µg/m2 increase in particulate matter concentrations. During the 7-year period, average particulate matter levels frequently exceeded World Health Organization (WHO) guideline values. A 10 µg/m2 increase in PM10 was associated with a 1.7% increase in daily mortality (RR: 1.017; 95% CI: 1.009-1.025), while a similar increase in PM2.5 was associated with a 3.3% increase (RR: 1.033; 95% CI: 1.021-1.046). Mortality increases were more pronounced among individuals aged ≥ 65 years. Periods of consecutive high pollution were also associated with excess mortality. Short-term increases in particulate matter concentrations were associated with elevated mortality in Istanbul, particularly among older adults. These results support the relevance of WHO guideline values in the local context and highlight the importance of sustained air quality control policies.
BACKGROUND
Air pollution is associated with anemia in children, however, longitudinal data supporting this association are insufficient.
METHODS
From 2019 to 2023, we conducted a dynamic cohort study involving 33,900 participants from 119 primary and secondary schools across 16 districts in Shanghai. We obtained the daily average concentrations of five air pollutants (PM2.5, O₃, NO₂, SO₂, and CO) based on school addresses using the China High Air Pollutants (CHAP) dataset to assess the exposure levels of the study subjects. We used latent class mixed models to determine the longitudinal trajectories of hemoglobin (Hb) and multinomial logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs) between trajectory categories. Linear and logistic regression models were used to evaluate the associations between air pollutant exposure level and Hb and anemia risk, respectively, and Cox regression models was used for longitudinal validation. Interaction terms for gender, age, and body mass index (BMI) were used to explore the modifying effects of these factors.
RESULTS
At the baseline survey, 3,213 students (9.48%) were identified as anemic, with a higher proportion of girls (63.8%). During an average follow-up period of 3.16 years, 1,685 participants (4.9%) were observed to develop anemia. Children's hemoglobin levels showed three different trajectory patterns throughout the study period. Exposure to PM2.5 [OR (95% CI) = 2.124(1.853, 2.433)] was associated with adverse trajectory changes characterized by "low hemoglobin". Longitudinal analysis shows that exposure to PM2.5 [HR = 1.213, 95% CI: (1.068, 1.376)], NO2 [HR = 1.409, 95% CI: (1.254, 1.584)], and SO2 [HR = 1.268, 95% CI: (1.172, 1.372)] is associated with an increased risk of anemia. Stratified analysis showed that the adverse effects of PM2.5 exposure on anemia were more pronounced in younger or underweight children. The adverse effects of NO2 exposure on anemia were more significant in older or obese children. The association between SO2 exposure and the impact on anemia mainly appeared in male or younger children.
CONCLUSIONS
Long-term exposure to air pollutants is associated with an increased burden of anemia in children and adolescents, and attention should be focused on vulnerable groups such as girls and underweight children.
K. Zheng, Fengyun Zhang, L. Chu et al.· BMC Public Health· 0 citations
Long-term exposure to air pollutants, particularly NO2 and PM10, is associated with an increased risk of microvascular complications among individuals with diabetes, and the observed risk appears to be persistent and may begin at relatively low exposure levels, underscoring the need for preventive strategies targeting environmental risk factors.