Objectives

Chromium VI (hexavalent chromium, Cr(VI)) is an established cause of lung cancer, but its association with gastrointestinal cancer is less clear. The goal of this study was to examine whether the current human epidemiological research on occupationally inhaled Cr(VI) supports the hypothesis that Cr(VI) is associated with human stomach cancer.

Methods

Following a thorough literature search and review of individual studies, we used meta-analysis to summarise the current epidemiological literature on inhaled Cr(VI) and stomach cancer, explore major sources of heterogeneity, and assess other elements of causal inference.

Results

We identified 56 cohort and case-control studies and 74 individual relative risk (RR) estimates on stomach cancer and Cr(VI) exposure or work in an occupation associated with high Cr(VI) exposure including chromium production, chrome plating, leather work and work with Portland cement. The summary RR for all studies combined was 1.27 (95% CI 1.18 to 1.38). In analyses limited to only those studies identifying increased risks of lung cancer, the summary RR for stomach cancer was higher (RR=1.41, 95% CI 1.18 to 1.69).

Conclusions

Overall, these results suggest that Cr(VI) is a stomach carcinogen in humans, which is consistent with the tumour results reported in rodent studies.

Objectives

We used an environmental justice screening tool (CalEnviroScreen 1.1) to compare the distribution of environmental hazards and vulnerable populations across California communities.

Methods

CalEnviroScreen 1.1 combines 17 indicators created from 2004 to 2013 publicly available data into a relative cumulative impact score. We compared cumulative impact scores across California zip codes on the basis of their location, urban or rural character, and racial/ethnic makeup. We used a concentration index to evaluate which indicators were most unequally distributed with respect to race/ethnicity and poverty.

Results

The unadjusted odds of living in one of the 10% most affected zip codes were 6.2, 5.8, 1.9, 1.8, and 1.6 times greater for Hispanics, African Americans, Native Americans, Asian/Pacific Islanders, and other or multiracial individuals, respectively, than for non-Hispanic Whites. Environmental hazards were more regressively distributed with respect to race/ethnicity than poverty, with pesticide use and toxic chemical releases being the most unequal.

Conclusions

Environmental health hazards disproportionately burden communities of color in California. Efforts to reduce disparities in pollution burden can use simple screening tools to prioritize areas for action.

Background

Assessing adverse effects from environmental chemical exposure is integral to public health policies. Toxicology assays identifying early biological changes from chemical exposure are increasing our ability to evaluate links between early biological disturbances and subsequent overt downstream effects. A workshop was held to consider how the resulting data inform consideration of an "adverse effect" in the context of hazard identification and risk assessment.

Objectives

Our objective here is to review what is known about the relationships between chemical exposure, early biological effects (upstream events), and later overt effects (downstream events) through three case studies (thyroid hormone disruption, antiandrogen effects, immune system disruption) and to consider how to evaluate hazard and risk when early biological effect data are available.

Discussion

Each case study presents data on the toxicity pathways linking early biological perturbations with downstream overt effects. Case studies also emphasize several factors that can influence risk of overt disease as a result from early biological perturbations, including background chemical exposures, underlying individual biological processes, and disease susceptibility. Certain effects resulting from exposure during periods of sensitivity may be irreversible. A chemical can act through multiple modes of action, resulting in similar or different overt effects.

Conclusions

For certain classes of early perturbations, sufficient information on the disease process is known, so hazard and quantitative risk assessment can proceed using information on upstream biological perturbations. Upstream data will support improved approaches for considering developmental stage, background exposures, disease status, and other factors important to assessing hazard and risk for the whole population.