About

Craig Steinmaus, MD, MPH, is an Adjunct Professor of Epidemiology at UC Berkeley Public Health. His research interests include arsenic in drinking water, perchlorate and thyroid hormones, and meta-analysis. He holds an MD from the University of California, Davis, an MPH from UC Berkeley, and a BS from UC Davis. His work has contributed to understanding the health impacts of environmental exposures, with publications on topics such as benzene and non-Hodgkin lymphoma and formaldehyde and brain disease.

Research topics

• Medicine
• Demography
• Pediatrics
• Internal medicine

Selected publications

• Arsenic exposure at birth, socioeconomic status, and epigenetic aging among adults in northern Chile

  Environmental Research · 2026-03-29

  articleOpen access

  Arsenic exposure remains a major global health concern, and early-life exposure has been linked to cancer, cardiovascular disease, and diabetes. Epigenetic biomarkers of aging may capture long-term effects of arsenic, yet whether exposure during sensitive developmental windows leaves detectable epigenetic signatures decades later remain unclear. Socioeconomic status (SES) may modify these relationships, yet its role as a modifier has not been examined. We leveraged a natural experiment in northern Chile, where municipal drinking-water arsenic concentrations were extremely high from 1958-1972. Decades later, leukocyte DNA methylation was measured among 358 adults (mean age = 65.7 years) using the Illumina EPIC v2 array. Arsenic concentration at birth (0-860μg/L) was assigned from historical water records. Current exposure was measured in urine (2-646μg/g creatinine). We evaluated associations of birth and current arsenic exposure with epigenome-wide methylation and epigenetic aging, incorporating multiplicative interaction and stratification by SES. No CpGs were linked to birth arsenic exposure, whereas nine CpGs passed the Bonferroni threshold for current urinary arsenic ( p Bonferroni <0.05). Each doubling of arsenic at birth was associated with older epigenetic age (Hannum: b = 0.11, 95% CI = 0.0027, 0.23; Zhang: 0.03, 0.00070, 0.06). SES modified associations for phenotypic age (PC-PhenoAge) and pace of aging (DunedinPACE) ( p interaction <0.05), especially among lower-SES individuals (PC-PhenoAge: b = 0.16, 95% CI = 0.02, 0.29; DunedinPACE: b = 0.0035, 95% CI = 0.00016, 0.0069). Early-life arsenic exposure was associated with accelerated epigenetic aging in adulthood, whereas current exposure was associated with CpG-specific methylation changes, particularly among socioeconomically disadvantaged individuals. • Higher arsenic at birth was linked to accelerated epigenetic aging decades later. • Epigenetic aging linked to arsenic at birth was evident in lower socioeconomic status. • Current arsenic exposure was associated with widespread CpG methylation changes. • Social disadvantage shaped epigenetic responses to arsenic across the life course.

  PublisherDOI

• Long-Term Effect of Early-Life Arsenic Exposure on Morning Plasma Cortisol in Adults from Antofagasta, Chile

  medRxiv · 2025-09-02

  preprintOpen access

  Over 100,000 people were exposed to arsenic-contaminated drinking water in Antofagasta, Chile from 1958-1970. Individuals born during this high exposure period have elevated rates of cancer, lung and cardiovascular disease, and hypertension. However, the mechanisms of long-term arsenic toxicity remain unclear. We investigated whether early-life arsenic exposure was associated with altered glucocorticoid levels in adulthood. This study included 114 individuals born in Antofagasta during the high exposure period and 118 individuals born elsewhere. Arsenic exposure metrics were constructed based on residential histories and included: concentration at birth, peak and highest 5-year average between ages 0-10 years, and highest lifetime 5-year average, and lifetime cumulative exposure. Morning plasma cortisol concentrations were measured using a cell-based bioassay. Individuals in the highest quartile of highest lifetime 5-year average of arsenic exposure had approximately 11% lower mean log cortisol levels than those in the lowest quartile of exposure (β = -0.116; 95% CI: -0.229, -0.003). In sex-stratified analyses, associations were stronger among females. For example, females in the highest quartile of cumulative exposure had 22.0% lower cortisol levels compared to those in the lowest quartile (β = -0.248; 95% CI: -0.444, -0.053) and the test for interaction by sex was statistically significant (p = 0.036). This study is the first to show that early-life arsenic exposure may have lasting effects on cortisol. These findings highlight endocrine disruption as a mechanism contributing to long-term health effects of early arsenic exposure.

  PublisherOA PDFDOI

• Evaluation of lung oxidative stress and inflammatory state using exhaled breath condensate analysis in early-life arsenic exposure

  Journal of Breath Research · 2025-09-09 · 1 citations

  articleOpen access

  Abstract Millions of people worldwide are exposed to environmental arsenic in drinking water, resulting in both malignant and nonmalignant diseases. Interestingly, early life exposure by itself is sufficient to produce higher incidences of these diseases later in life. Based on the delayed onset of disease, we hypothesized that early life arsenic exposure would also induce long-term alterations in the metabolic profile. The objective of this study was to examine metabolomic biomarkers in exhaled breath condensate (EBC) of individuals exposed to arsenic in drinking water early in life, but not later. One hundred and fifty subjects (75 males and 75 females) were initially recruited from Antofagasta, Chile, some of whom were exposed to high water arsenic levels (⩾870 µ g l −1 ; HighAE group), and others, low water arsenic levels (⩽110 µ g l −1 ; LowAE group) early in life (1958–1970). EBC samples were collected for targeted and untargeted metabolomic biomarker analysis. The results showed significantly shorter individuals and reduced pulmonary functions (forced vital capacity, FVC and forced expiratory volume in 1 s, FEV 1 ) in both males and females in the high-arsenic groups. Males exposed to high arsenic levels also had reduced red blood cell concentrations, as well as higher concentrations of the oxidative stress metabolites 8-OH-2dG and 8-iso-PGF2 α . Females in the high-arsenic group showed reductions in 8-OH-2dG. Untargeted analysis revealed metabolomic markers that differentiated the HighAE group from the LowAE group, with a subgroup of markers whose concentrations were proportional to the level of arsenic exposure. Targeted and untargeted analyses of EBC using liquid chromatography–mass spectrometry indicated that adults exposed to high arsenic levels in drinking water in utero and during early childhood retained a modified metabolic profile 47 years after the end of exposure.

  PublisherDOI

• Arsenic in drinking water and breast cancer: a case–control study from a high exposure area in Northern Chile

  Breast Cancer Research and Treatment · 2025-07-08 · 1 citations

  article
  PublisherDOI

• Arsenic in Drinking Water and Prostate Cancer: A Population-Based Case–Control Study in Northern Chile

  Cancer Epidemiology Biomarkers & Prevention · 2025-09-16 · 1 citations

  articleSenior author

  BACKGROUND: Epidemiologic evidence demonstrates increased lung, bladder, and skin cancer risk among individuals exposed to arsenic in drinking water. Some studies report associations with prostate cancer, but data are limited. This study aimed to examine the association between arsenic in drinking water and prostate cancer in Northern Chile. With its wide range of exposure (<10-860 µg/L), large population, and accurate information on historic exposures, Northern Chile is the best place to investigate the human carcinogenic effects of arsenic. METHODS: A case-control study conducted from 2015 to 2019 enrolled 343 prostate cancer cases and 337 age-matched controls among men ages ≥40 years. Cases were ascertained from cancer committees, hospitals, and medical facilities in the area. Controls were ascertained from the Chile Voter Registry, including >90% of adults ages >50 years. Information on lifetime arsenic exposure and potential confounders such as smoking, family history, and prostate cancer screening were collected. RESULTS: Twenty-three percent of participants were exposed to arsenic concentrations >800 µg/L in their lifetime (80× recommended thresholds). Cases and controls were demographically similar. After adjustment for age and smoking status, participants with the highest quartile of lifetime cumulative and average arsenic concentrations in drinking water each had 1.14 (95% confidence interval, 0.71-1.84) and 1.17 (95% confidence interval, 0.73-1.89) times the odds of prostate cancer compared with participants with the lowest quartile of exposure, respectively. CONCLUSIONS: Arsenic exposure in drinking water, even at high levels, was not associated with increased risk of prostate cancer. IMPACT: Our findings suggest that arsenic is not a risk factor for prostate cancer.

  PublisherDOI

• Supplementary Table 2 from Drinking Water Arsenic in Northern Chile: High Cancer Risks 40 Years after Exposure Cessation

  2023-03-31

  supplementary-materialsOpen access1st authorCorresponding

  &lt;p&gt;PDF file - 31K - Bladder and lung cancer odds ratios including only cases with histologic confirmation, in non-proxy subjects, and in males and females comparing subjects in the upper to lower quartiles of average lifetime arsenic concentration prior to 1971 (the end of the high exposure period in Antofagasta)&lt;/p&gt;

  PublisherDOI

• S17-02: The Long-term Impact of Perinatal Exposures on Susceptibility to Immune-mediated Diseases

  Toxicology Letters · 2023-09-01

  article
  PublisherDOI

• Supplementary Table 1 from Drinking Water Arsenic in Northern Chile: High Cancer Risks 40 Years after Exposure Cessation

  2023-03-31

  supplementary-materialsOpen access1st authorCorresponding

  &lt;p&gt;PDF file - 26K - Arsenic concentration and intake metrics in bladder and lung cancer cases and controls&lt;/p&gt;

  PublisherDOI

• Data from Increased Lung and Bladder Cancer Incidence in Adults after &lt;i&gt;In Utero&lt;/i&gt; and Early-Life Arsenic Exposure

  2023-03-31

  preprintOpen access1st authorCorresponding

  &lt;div&gt;Abstract&lt;p&gt;&lt;b&gt;Background:&lt;/b&gt; From 1958 to 1970, &gt;100,000 people in northern Chile were exposed to a well-documented, distinct period of high drinking water arsenic concentrations. We previously reported ecological evidence suggesting that early-life exposure in this population resulted in increased mortality in adults from several outcomes, including lung and bladder cancer.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Methods:&lt;/b&gt; We have now completed the first study ever assessing incident cancer cases after early-life arsenic exposure, and the first study on this topic with individual participant exposure and confounding factor data. Subjects included 221 lung and 160 bladder cancer cases diagnosed in northern Chile from 2007 to 2010, and 508 age and gender-matched controls.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Results:&lt;/b&gt; ORs adjusted for age, sex, and smoking in those only exposed in early life to arsenic water concentrations of ≤110, 110 to 800, and &gt;800 μg/L were 1.00, 1.88 [95% confidence interval (CI), 0.96–3.71], and 5.24 (3.05–9.00; &lt;i&gt;P&lt;/i&gt;&lt;sub&gt;trend&lt;/sub&gt; &lt; 0.001) for lung cancer, and 1.00, 2.94 (1.29–6.70), and 8.11 (4.31–15.25; &lt;i&gt;P&lt;/i&gt;&lt;sub&gt;trend&lt;/sub&gt; &lt; 0.001) for bladder cancer. ORs were lower in those not exposed until adulthood. The highest category (&gt;800 μg/L) involved exposures that started 49 to 52 years before, and ended 37 to 40 years before the cancer cases were diagnosed.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Conclusion:&lt;/b&gt; Lung and bladder cancer incidence in adults was markedly increased following exposure to arsenic in early life, even up to 40 years after high exposures ceased. Such findings have not been identified before for any environmental exposure, and suggest that humans are extraordinarily susceptible to early-life arsenic exposure.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Impact:&lt;/b&gt; Policies aimed at reducing early-life exposure may help reduce the long-term risks of arsenic-related disease. &lt;i&gt;Cancer Epidemiol Biomarkers Prev; 23(8); 1529–38. ©2014 AACR&lt;/i&gt;.&lt;/p&gt;&lt;/div&gt;

  PublisherDOI

• Supplementary Tables 1 through 3 from Increased Lung and Bladder Cancer Incidence in Adults after &lt;i&gt;In Utero&lt;/i&gt; and Early-Life Arsenic Exposure

  2023-03-31

  supplementary-materialsOpen access1st authorCorresponding

  &lt;p&gt;PDF - 115K, Table S1. Comparison of subjects included in this analysis to subjects excluded because they had high exposures both in early life and adulthood. Table S2. Comparison of residences of the Chile case control study controls at the time of ascertainment to the 2002 Chile census. Table S3. Cancer odds ratios in subjects exposed in utero and childhood using different age categories to define early-life exposure.&lt;/p&gt;

  PublisherDOI

Recent grants

• PERCHLORATE AND THYROID HORMONES IN PREGNANCY AND INFANTS IN SOUTHERN CALIFORNIA

  NIH · $2.1M · 2011–2016

• NIH Grant K23ES011133

  NIH · $607k · 2006

• NIH Grant R01ES017463

  NIH · $1.3M · 2013

• In situ destruction of halogenated Superfund contaminants with persulfate-generated radicals

  NIH · $84.5M · 1997–2027

• Cancer in adults following in utero and early life exposure to arsenic

  NIH · $3.8M · 2007–2021

Frequent coauthors

• Allan H. Smith

  St. Vincent Hospital

  165 shared

• Catterina Ferreccio

  Instituto de Salud Pública de Chile

  103 shared

• Jane Liaw

  102 shared

• John R. Balmes

  University of California, Berkeley

  52 shared

• Guillermo Marshall

  University of British Columbia

  45 shared

• Yan Yuan

  44 shared

• Johanna Acevedo

  Universidad del Desarrollo del Estado de Puebla

  35 shared

• Yan Yuan

  China Pharmaceutical University

  35 shared