Long-term impact of Hurricane Maria on point-of-use drinking water quality in Puerto Rico and associated potential adverse health effects.

Drinking water security in Puerto Rico (PR) is increasingly challenged by both regulated and emerging anthropogenic contaminants, which was exacerbated by the Hurricane Maria (HM) due to impaired regional water cycle and damaged water infrastructure. Leveraging the NIEHS PROTECT (Puerto Rico Testsite for Exploring Contamination Threats) cohort, this study assessed the long-term tap water (TW) quality changes from March 2018 to November 2018 after HM in PR, by innovatively integrating two different effect-based quantitative toxicity assays with a targeted analysis of 200 organic and 22 inorganic pollutants. Post-hurricane PR TW quality showed recovery after >6-month period as indicated by the decreased number of contaminants showing elevated average concentrations relative to pre-hurricane samples, with significant difference of both chemical and toxicity levels between northern and southern PR. Molecular toxicity profiling and correlation revealed that the HM-accelerated releases of certain pesticides and PPCPs could exert increased cellular oxidative and/or AhR (aryl hydrocarbon receptor)-mediated activities that may persist for more than six months after HM. Maximum cumulative ratio and adverse outcome pathway (AOP) assessment identified the top ranked detected TW contaminants (Cu, Sr, V, perfluorooctanoic acid) that potentially associated with different adverse health effects such as inflammation, impaired reproductive systems, cancers/tumors, and/or organ toxicity. These insights can be incorporated into the regulatory framework for post-disaster risk assessment, guiding water quality control and management for public health protection.

Impact of Hurricane Maria on Drinking Water Quality in Puerto Rico.

This study performed a comprehensive assessment of the impact of Hurricane Maria (HM) on drinking water quality in Puerto Rico (PR) by integrating targeted chemical analysis of both inorganic (18 trace elements) and organic trace pollutants (200 micropollutants) with high-throughput quantitative toxicogenomics and in vitro biomarkers-based toxicity assays. Average concentrations of 14 detected trace elements and 20 organic micropollutants showed elevation after HM. Arsenic, sucralose, perfluorooctanoic acid (PFOA), atrazine-2-hydroxy, benzotriazole, acesulfame, and prometon were at significantly (p < 0.05) higher levels in the post-HM than in the pre-HM samples. Thirteen micropollutants, including four pesticides, were only detected in posthurricane samples. Spatial comparison showed higher pollutant and toxicity levels in the samples from northern PR (where eight Superfund sites are located) than in those from southern PR. Distinctive pathway-specific molecular toxicity fingerprints for water extracts before and after HM and at different locations revealed changes in toxicity nature that likely resulted from the impact of HM on drinking water composition. Correlation analysis and Maximum Cumulative Ratio assessment suggested that metals (i.e., arsenic) and PFOA were the top ranked pollutants that have the potential to cause increased risk after HM, providing a possible direction for future water resource management and epidemiological studies.

DNA adducts in granulocytes of hospital workers exposed to ethylene oxide.

BACKGROUND: Ethylene oxide (EtO), an important industrial chemical intermediate and sterilant, is classified as a human carcinogen. Occupational EtO exposure in many countries is regulated at 1 ppm (8-hr TWA), but levels of EtO-DNA adducts in humans with low occupational EtO exposures have not been reported. METHODS: We examined the formation of N7-(2'-hydroxyethyl)guanine (N7-HEG), a major DNA adduct of EtO, in 58 EtO-exposed sterilizer operators and six nonexposed workers from ten hospitals. N7-HEG was quantified in granulocyte DNA (0.1-11.5 microg) by a highly sensitive and specific gas chromatography-electron capture-mass spectrometry method. Cumulative exposure to EtO (ppm-hour) was estimated during the 4-month period before the collection of blood samples. RESULTS: There was considerable inter-individual variability in the levels of N7-HEG with a range of 1.6-241.3 adducts/10(7) nucleotides. The mean levels in the nonexposed, low (< or =32 ppm-hour), and high (>32 ppm-hour) EtO-exposure groups were 3.8, 16.3, and 20.3 adducts/10(7) nucleotides, respectively, after the adjustment for cigarette smoking and other potential confounders, but the differences were not statistically significant. CONCLUSIONS: This study has demonstrated for the first time, detectable levels of N7-HEG adducts in granulocytes of hospital workers with EtO exposures at levels less than the current U.S. standard of 1 ppm (8-hr TWA). A nonsignificant increase in adduct levels with increasing EtO exposure indicates that further studies of EtO-exposed workers are needed to clarify the relationship between EtO exposure and N7-HEG adduct formation.