Concentrations of the genotoxic metals, chromium and nickel, in whales, tar balls, oil slicks, and released oil from the gulf of Mexico in the immediate aftermath of the deepwater horizon oil crisis: is genotoxic metal exposure part of the deepwater horizon legacy?

Concern regarding the Deepwater Horizon oil crisis has largely focused on oil and dispersants while the threat of genotoxic metals in the oil has gone largely overlooked. Genotoxic metals, such as chromium and nickel, damage DNA and bioaccumulate in organisms, resulting in persistent exposures. We found chromium and nickel concentrations ranged from 0.24 to 8.46 ppm in crude oil from the riser, oil from slicks on surface waters and tar balls from Gulf of Mexico beaches. We found nickel concentrations ranged from 1.7 to 94.6 ppm wet weight with a mean of 15.9 ± 3.5 ppm and chromium concentrations ranged from 2.0 to 73.6 ppm wet weight with a mean of 12.8 ± 2.6 ppm in tissue collected from Gulf of Mexico whales in the wake of the crisis. Mean tissue concentrations were significantly higher than those found in whales collected around the world prior to the spill. Given the capacity of these metals to damage DNA, their presence in the oil, and their elevated concentrations in whales, we suggest that metal exposure is an important understudied concern for the Deepwater Horizon oil disaster.

The association of PM(2.5) with full term low birth weight at different spatial scales.

There is interest in determining the relationship between fine particulate matter air pollution and various health outcomes, including birth outcomes such as term low birth weight. Previous studies have come to different conclusions. In this study we consider whether the effect may vary by location and gestational period. We also compare results when using different spatial resolutions for the air concentration estimates. Among the seven states considered, New Jersey and New York had the highest PM2.5 levels (average full gestation period exposures of 13 µg/m(3)) and the largest rate of low birth weight births (2.6 and 2.8%, respectively); conversely Utah and Minnesota had the lowest PM2.5 levels (9 µg/m(3)) and the lowest rates of low birth weight births (2.1 and1.9%, respectively). There is an association between PM2.5 exposure and low birth weight in New York for the full gestation period and all three trimesters, in Minnesota for the full gestation period and the first and third trimesters, and in New Jersey for the full gestation period and the first trimester. When we pooled the data across states, the OR for the full gestation period was 1.030 (95% CI: 1.022-1.037) and it was highest for the first trimester (OR 1.018; CI: 1.013-1.022) and decreasing during the later trimesters. When we used a finer spatial resolution, the strengths of the associations tended to diminish and were no longer statistically significant. We consider reasons why these differences may occur and their implications for evaluating the effects of PM2.5 on birth outcomes.

Excising squamous cell carcinomas: comparing the performance of GPs, hospital skin specialists and other hospital specialists.

BACKGROUND: GPs have no defined role in the excision of squamous cell carcinomas (SCCs). Current guidelines recommend that all skin lesions suspicious of SCC should be referred urgently to secondary care. Evidence regarding current management of SCC in primary care is limited. Existing audit data suggest that up to 10% of SCCs may be excised in primary care. GPs may be able to have a greater role in the management of SCC but more evidence is required before this can be advocated. OBJECTIVE: To compare the practice of GPs, skin specialists (dermatologists and plastic surgeons) and other hospital specialists in excising SCCs. Methods . A retrospective analysis of all SCCs excised in the Grampian region between 1 January and 31 December 2005. A total of 1184 reports were rated for source and adequacy of excision. RESULTS: GPs excised 23.7% of all SCC-positive biopsies. Whether the biopsy had been performed by a GP or a hospital skin specialist made no significant difference to excision adequacy. However, GPs were significantly more likely to excise adequately than hospital non-specialists (P < 0.001). Infrequent GP excisers appear to perform as well as frequent excisers in adequately excising SCCs. CONCLUSIONS: GPs excise a considerable number of SCCs in primary care. GPs compare favourably to skin specialists in excising SCCs. The performance of infrequent GP excisers does not appear to differ significantly from that of frequent GP excisers. Further work is required to define more clearly the role of GPs in the management of SCCs.

Depleted uranium induces neoplastic transformation in human lung epithelial cells.

Depleted uranium (DU) is commonly used in military armor and munitions, and thus, exposure of soldiers and noncombatants is frequent and widespread. Previous studies have shown that DU has both chemical and radiological toxicity and that the primary route of exposure of DU to humans is through inhalation and ingestion. However, there is limited research information on the potential carcinogenicity of DU in human bronchial cells. Accordingly, we determined the neoplastic transforming ability of particulate DU to human bronchial epithelial cells (BEP2D). We observed the loss of contact inhibition and anchorage independent growth in cells exposed to DU after 24 h. We also characterized these DU-induced transformed cell lines and found that 40% of the cell lines exhibit alterations in plating efficiency and no significant changes in the cytotoxic response to DU. Cytogenetic analyses showed that 53% of the DU-transformed cell lines possess a hypodiploid phenotype. These data indicate that human bronchial cells are transformed by DU and exhibit significant chromosome instability consistent with a neoplastic phenotype.

Comparative genotoxicity and cytotoxicity of four hexavalent chromium compounds in human bronchial cells.

Hexavalent chromium (Cr(VI)) compounds are well-established human lung carcinogens. Solubility plays an important role in their carcinogenicity with the particulate Cr(VI) compounds being the most carcinogenic. Epidemiology and animal studies suggest that zinc chromate is the most potent particulate Cr(VI) compound; however, there are few comparative data to support these observations. The purpose of this study was to compare the genotoxicity of zinc chromate with two other particulate Cr(VI) compounds, barium chromate and lead chromate, and one soluble Cr(VI) compound, sodium chromate. The clastogenic effects of barium chromate and zinc chromate were similar, but lead chromate induced significantly less damage. The levels of DNA damage measured by gamma-H2A.X foci formation were similar for the three particulate chromium compounds. Corrected for chromium uptake differences, we found that zinc chromate and barium chromate were the most cytotoxic, and lead chromate and sodium chromate were less cytotoxic. Zinc chromate was more clastogenic than all other chromium compounds, and lead chromate was the least clastogenic. There was no significant difference between any of the compounds for the induction of DNA double strand breaks. All together, these data suggest that the difference in the carcinogenic potency of zinc chromate over the other chromium compounds is not due solely to a difference in chromium ion uptake and that the zinc cation may in fact have an important role in its carcinogenicity.

Privacy versus public health: the impact of current confidentiality rules.

Public health research and practice often have been facilitated through the evaluation and study of population-based data collected by local, state, and federal governments. However, recent concerns about identify theft, confidentiality, and patient privacy have led to increasingly restrictive policies on data access, often preventing researchers from using these valuable data. We believe that these restrictions, and the research impeded or precluded by their implementation and enforcement, have had a significant negative impact on important public health research. Members of the public health community should challenge these policies through their professional societies and by lobbying legislators and health officials to advocate for changes that establish a more appropriate balance between privacy concerns and the protection of public health.

Birth and fetal death records and environmental exposures: promising data elements for environmental public health tracking of reproductive outcomes.

OBJECTIVES: We inventoried and reviewed the birth and fetal death certificates of all 50 U.S. states to identify nonstandard data items that are environmentally relevant, inexpensive to collect, and might enhance environmental public health tracking. METHODS: We obtained online or requested by mail or telephone the birth certificate and fetal death record forms or formats from each state. Every state data element was compared to the 2003 standards promulgated by the National Center for Health Statistics to identify any items that are not included on the standard. We then evaluated these items for their utility in environmentally related analyses. RESULTS: We found three data fields of potential interest. First, although every state included residence of mother at time of delivery on the birth certificate, only four states collected information on how long the mother had lived there. This item may be useful in that it could be used to assess and reduce misclassification of environmental exposures among women during pregnancy. Second, we found that father's address was listed on the birth certificates of eight states. This data field may be useful for defining paternal environmental exposures, especially in cases where the parents do not live together. Third, parental occupation was listed on the birth certificates of 15 states and may be useful for defining parental workplace exposures. Our findings were similar for fetal death records. CONCLUSION: If these data elements are accurate and well-reported, their addition to birth, fetal death, and other health records may aid in environmental public health tracking.

Similar asthma prevalence estimates obtained from preadolescent and parent survey responses.

OBJECTIVE: We compared agreement between child and parent responses to questions assessing prevalence of asthma and other severe respiratory symptoms. STUDY DESIGN AND SETTING: Fifth-grade children enrolled in public schools and their parents separately completed a health survey, which included respiratory symptom questions from the International Study of Asthma and Allergies in Childhood (ISAAC). Agreement on respiratory symptom questions was assessed with Cohen's Kappa coefficient. Asthma prevalence estimates based on responses to several questions were also compared using child and parent data. The analysis was based on a study sample size of 230 matched parent and child questionnaires. RESULTS: High levels of agreement (Kappa: 0.76 and 0.79) between child and parent responses were observed for current and lifetime asthma, and similar asthma prevalence estimates were obtained from child and parent response data. Five of the questions on potentially severe respiratory symptoms had low to fair levels of agreement (Kappa: -0.01 to 0.38), resulting in statistically significantly different prevalence estimates in three of the five symptoms. CONCLUSIONS: Separate parent and child responses to a series of respiratory symptom and asthma questions yielded similar estimates for asthma prevalence but different estimates for the prevalence of several severe respiratory symptoms.

Hexavalent chromium is cytotoxic and genotoxic to the North Atlantic right whale (Eubalaena glacialis) lung and testes fibroblasts.

Although hexavalent chromium is a known genotoxic agent in human and terrestrial mammals and is present in seawater and air, its effects on marine mammals including the endangered North Atlantic right whale are unknown and untested. The present study investigated the cytotoxic and genotoxic effects of hexavalent chromium in primary cultured North Atlantic right whale lung and testes fibroblasts and levels of total chromium in skin biopsies from North Atlantic right whales. Cytotoxicity was measured by clonogenic survival assay. Genotoxicity was measured as production of chromosome aberrations. Tissue chromium levels were determined from skin biopsies of healthy free-ranging whales in the Bay of Fundy using inductively coupled plasma optical emission spectroscopy. Hexavalent chromium-induced concentration-dependent increases in right whale lung and testes fibroblast cytotoxicity with the testes more sensitive to the cytotoxic effects. It also induced concentration-dependent increases in chromosomal aberrations in both cell types with no significant difference in sensitivity. Skin biopsy data indicate that North Atlantic right whales are exposed to chromium and accumulate a range of 4.9-10 microg Cr/g tissue with a mean of 7.1 microg/g. Hexavalent chromium is cytotoxic and genotoxic to North Atlantic right whale cells. The whales have tissue chromium levels that are concerning. These data support a hypothesis that chromium may be a concern for the health of the North Atlantic right whales. Considering these data with chromium chemistry, whale physiology and atmospheric chromium levels further suggest that inhalation may be an important exposure route.

The cytotoxicity and genotoxicity of hexavalent chromium in medaka (Oryzias latipes) cells.

Chromium is an increasing health concern for aquatic environments, however, the mechanism of chromium toxicity in aquatic species is yet unknown. We used a medaka (Oryzias latipes) fin cell line to investigate the cytotoxicity and genotoxicity of sodium chromate, a soluble form of hexavalent chromium. We used a clonogenic cytotoxicity assay to measure sodium chromate cytotoxicity, gamma-H2A.X immunofluoresence to measure DNA double-strand breaks, and chromosome damage to measure clastogenicity. We found that sodium chromate is cytotoxic to medaka fin cells, with toxicity increasing in a concentration-dependent manner. Treatments of 0.5, 1, 5, 10, 25, 50 and 100 microM sodium chromate caused 100, 103.5, 87.8, 77.5, 40.9, 15 and 2.7% survival, respectively, relative to the control. We visualized DNA double-strand breaks in medaka cells through the formation of gamma-H2A.X foci. Breaks could be detected at concentrations as low as 1 microM. We also found that sodium chromate induces chromosomal aberrations, causing chromatid lesions and exchanges that increase with concentration. Treatments of 0, 1, 5, 10 and 25 microM sodium chromate damaged 10.3, 17, 32.3, 43 and 51.6% of metaphases and induced 13, 23, 44, 69 and 118 total aberrations in 100 metaphases, respectively. These data show that hexavalent chromium is both cytotoxic and genotoxic to fish cells. Our results set the context for future work in the medaka cell culture model and provide important tools for investigating mechanisms of toxicity in aquatic organisms.

Developing integrated multistate environmental public health surveillance.

Environmental exposures cause substantial morbidity and mortality in the United States. A major goal of Centers for Disease Control and Prevention Environmental Public Health Tracking program is the development of a national network of health and environmental data with analytic tools for rapid evaluation of specific national or regional environmental health concerns. A six-state collaborative project in the northeast United States was established to assess the feasibility of such a system, assessing the possible association between ambient air quality and adverse birth outcomes. For this regional surveillance project, issues were discussed surrounding the design of a mutually acceptable protocol, obtaining human subjects' protection approvals, obtaining and organizing both the exposure and outcome data, analyzing the data both locally and regionally, and planning subsequent interventions to address identified public health concerns.

Chronic exposure to lead chromate causes centrosome abnormalities and aneuploidy in human lung cells.

Hexavalent chromium [Cr(VI)] compounds are established human lung carcinogens. The carcinogenicity of Cr(VI) is related to its solubility, with the most potent carcinogens being the insoluble particulate Cr(VI) compounds. However, it remains unknown why particulate Cr(VI) is more carcinogenic than soluble Cr(VI). One possible explanation is that particulates may provide more chronic exposures to chromate over time. We found that aneuploid cells increased in a concentration- and time-dependent manner after chronic exposure to lead chromate. Specifically, a 24-hour lead chromate exposure induced no aneugenic effect, whereas a 120-hour exposure to 0.5 and 1 microg/cm2 lead chromate induced 55% and 60% aneuploid metaphases, respectively. We also found that many of these aneuploid cells were able to continue to grow and form colonies. Centrosome defects are known to induce aneuploidy; therefore, we investigated the effects of chronic lead chromate exposure on centrosomes. We found that centrosome amplification in interphase and mitotic cells increased in a concentration- and time-dependent manner with 0.5 and 1 microg/cm2 lead chromate for 120 hours, inducing aberrant centrosomes in 18% and 21% of interphase cells and 32% and 69% of mitotic cells, respectively; however, lead oxide did not induce centrosome amplification in interphase or mitotic cells. There was also an increase in aberrant mitosis after chronic exposure to lead chromate with the emergence of disorganized anaphase and mitotic catastrophe. These data suggest that one possible mechanism for lead chromate-induced carcinogenesis is through centrosome dysfunction, leading to the induction of aneuploidy.

Homologous recombination repair protects against particulate chromate-induced chromosome instability in Chinese hamster cells.

Particulate hexavalent chromium [Cr(VI)] compounds are well-established human carcinogens. Cr(VI)-induced tumors are characterized by chromosomal instability (CIN); however, the mechanisms of this effect are unknown. We investigated the hypothesis that homologous recombination (HR) repair of DNA double-strand breaks protect cells from Cr(VI)-induced CIN by focusing on the XRCC3 and RAD51C genes, which play an important role in cellular resistance to DNA double-strand breaks. We used Chinese hamster cells defective in each HR gene (irs3 for RAD51C and irs1SF for XRCC3) and compared with their wildtype parental and cDNA-complemented controls. We found that the intracellular Cr ion levels varied among the cell lines after particulate chromate treatment. Importantly, accounting for differences in Cr ion levels, we discovered that XRCC3 and RAD51C cells treated with lead chromate had increased cytotoxicity and chromosomal aberrations, relative to wildtype and cDNA-complimented cells. We also observed the emergence of high levels of chromatid exchanges in the two mutant cell lines. For example, 1microg/cm(2) lead chromate induced 20 and 32 exchanges in XRCC3- and RAD51C-deficient cells, respectively, whereas no exchanges were detected in the wildtype and cDNA-complemented cells. These observations suggest that HR protects cells from Cr(VI)-induced CIN, consistent with the ability of particulate Cr(VI) to induce double-strand breaks.

Role of the Fancg gene in protecting cells from particulate chromate-induced chromosome instability.

Particulate hexavalent chromium (Cr(VI)) is a known human lung carcinogen. Cr(VI)-induced tumors exhibit chromosome instability (CIN), but the mechanisms underlying these effects are unknown. We investigated a possible role for the Fanconi anemia (FA) pathway in particulate Cr(VI)-induced chromosomal damage by focusing on the Fancg gene, which plays an important role in cellular resistance to DNA interstrand crosslinks. We used the isogenic Chinese hamster ovary (CHO) KO40 fancg mutant compared with parental and gene-complemented cells. We found that fancg cells treated with lead chromate had lower intracellular Cr ion levels than control cell lines. Accounting for differences of Cr ion levels between cell lines, we discovered that fancg cells treated with lead chromate had increased cytotoxicity and chromosomal aberrations, which was not observed after restoring the Fancg gene. Chromosomal damage was manifest as increased total chromosome damage and percent metaphases with damage, specifically an increase in chromatid and isochromatid breaks. We conclude that Fancg protects cells from particulate Cr(VI)-induced cytotoxicity and chromosome damage, which is consistent with the known sensitivity of fancg cells to crosslinking damage and the ability of Cr(VI) to produce crosslinks.

Developmental delays and locomotor activity in the C57BL6/J mouse following neonatal exposure to the fully-brominated PBDE, decabromodiphenyl ether.

After several decades of commercial use, the flame retardant chemicals polybrominated diphenyl ethers (PBDEs) and their metabolites have become pervasive environmental contaminants with a global distribution. PBDEs have entered the food chain and increasing levels can be detected in the human body. Decabrominated diphenyl ether (decaBDE) is currently the most widely used of the PBDEs in the United States. Despite its widespread use, little is known about the health effects of decaBDE. The current study examined the effects of neonatal exposure to decaBDE in the inbred C57BL6/J mouse. Neonatal male and female mice were exposed to a daily oral dose of 0, 6, or 20 mg/kg decaBDE from postnatal day 2 to 15. Three groups of endpoints were examined: the ontogeny of sensorimotor responses and serum thyroxine levels in immature animals, and locomotor activity in adult animals. In immature animals, 20 mg/kg/day produced developmental delays in the acquisition of the palpebral reflex. At this age, exposed males also showed a dose-related reduction of serum thyroxine levels. As adults, decaBDE exposure altered the normal sex- and age-specific characteristics of spontaneous locomotor activity. The most striking effect was an increase of activity during the first 1.5 h of the 2 h assessment in males exposed to 20 mg/kg/day decaBDE. These effects suggest that decaBDE is a developmental neurotoxicant that can produce long-term behavioral changes following a discrete period of neonatal exposure.

XRCC1 protects against particulate chromate-induced chromosome damage and cytotoxicity in Chinese hamster ovary cells.

Water-insoluble hexavalent chromium compounds are well-established human lung carcinogens. Lead chromate, a model insoluble Cr(VI) compound, induces DNA damage, chromosome aberrations, and dose-dependent cell death in human and Chinese hamster ovary (CHO) cells. The relationship between lead chromate-induced DNA damage and chromosome aberrations is unknown. Our study focus was on examining the role of XRCC1 in lead chromate-induced cytotoxicity and structural chromosomal aberrations in CHO cells. Three different cell lines were used: AA8 (parental), EM9 (XRCC1 mutant), and H9T3 (EM9 complemented with human XRCC1 gene). Cytotoxicity was significantly higher in EM9 cells when compared to AA8 and H9T3 cells, indicating that XRCC1 is important for protecting cells from lead chromate particles-induced cell death. The frequency of damaged metaphase cells was not affected by XRCC1 deficiency. However, the total amount of Cr(VI)-induced chromosome damage was exacerbated by XRCC1 deficiency, and the spectrum of damage changed dramatically. Chromatid and isochromatid lesions were the most prominent aberrations induced in all cell lines. XRCC1 was essential to reduce the formation of chromatid lesions but not for isochromatid lesions. In addition, XRCC1 deficiency resulted in a dramatic increase in the number of chromatid exchanges, indicating that XRCC1 is involved in protection from lead chromate-induced chromosome instability.

XRCC1 protects against particulate chromate-induced chromosome damage and cytotoxicity in Chinese hamster ovary cells.

Water-insoluble hexavalent chromium compounds are well-established human lung carcinogens. Lead chromate, a model insoluble Cr(VI) compound, induces DNA damage, chromosome aberrations, and dose-dependent cell death in human and Chinese hamster ovary (CHO) cells. The relationship between lead chromate-induced DNA damage and chromosome aberrations is unknown. Our study focus was on examining the role of XRCC1 in lead chromate-induced cytotoxicity and structural chromosomal aberrations in CHO cells. Three different cell lines were used: AA8 (parental), EM9 (XRCC1 mutant), and H9T3 (EM9 complemented with human XRCC1 gene). Cytotoxicity was significantly higher in EM9 cells when compared to AA8 and H9T3 cells, indicating that XRCC1 is important for protecting cells from lead chromate particles-induced cell death. The frequency of damaged metaphase cells was not affected by XRCC1 deficiency. However, the total amount of Cr(VI)-induced chromosome damage was exacerbated by XRCC1 deficiency, and the spectrum of damage changed dramatically. Chromatid and isochromatid lesions were the most prominent aberrations induced in all cell lines. XRCC1 was essential to reduce the formation of chromatid lesions, but not for isochromatid lesions. In addition, XRCC1 deficiency resulted in a dramatic increase in the number of chromatid exchanges, indicating that XRCC1 is involved in protection from lead chromate-induced chromosome instability.

Thrombosis and neointima formation in vein grafts are inhibited by locally applied aspirin through endothelial protection.

Vein graft failure within the first month after bypass surgery is largely because of thrombosis. However, systemic study of thrombus formation in vein grafts is still lacking, and few effective techniques are available to prevent this event. Herein, we analyzed the kinetics of thrombosis and tested the effectiveness of locally applied aspirin on prevention of the disease in a mouse model. En face analysis of vein grafts revealed that 67+/-12% and 54+/-17% of the surface areas were covered by microthrombi at 1 and 3 days, respectively. Thrombus generation was also identified by labeling of platelets and fibrin, which occurred in 35 grafts examined at 1 and 3 days and 1, 2, 4, and 8 weeks. In a fifth of grafts, the thrombus occluded the vessel lumen by > or =1/4. Furthermore, a significant loss of endothelial cells was evidenced by beta-gal staining for vein grafts in transgenic mice expressing LacZ gene controlled by TIE2-endothelial specific gene promoter. Following thrombosis, neointimal lesions were significantly increased by 4-fold 2 weeks after the operation. When vein grafts were treated locally with aspirin in pluronic gel-127, the thrombus area was significantly reduced (P<0.005) at 1, 4, and 8 weeks. Interestingly, neointimal lesions were markedly reduced in the local, but not oral, aspirin-treated group at 4 and 8 weeks by 50% to 70% (P<0.005). The mechanism of reduced lesions by locally applied aspirin involved the protection of vein graft endothelium. Thus, we provide strong evidence that thrombus formation occurs before the development of neointimal lesions in vein grafts and that local aspirin treatment successfully reduces vein graft arteriosclerosis through endothelial protection, resulting in reduction of thrombosis.

XRCC1 protects cells from chromate-induced chromosome damage, but does not affect cytotoxicity.

Hexavalent chromium Cr(VI) is a well known human carcinogen. This genotoxic metal induces DNA strand breaks and chromosome damage. However, the relationship between these lesions is uncertain. Our study focused on examining the role of XRCC1 in sodium chromate-induced cytotoxicity and chromosomal aberrations in Chinese Hamster Ovary (CHO) cells. Three different cell lines were used: AA8 (parental), EM9 (XRCC1 mutant) and H9T3 (EM9 complemented with human XRCC1 gene). Results show that concentration-dependent decreases in relative survival are similar in all three cell lines, indicating that XRCC1 is not crucial for protecting cells from sodium chromate-induced cytotoxicity. Similarly the frequency of damaged metaphase cells was not affected by XRCC1 deficiency. However, the total number of Cr(VI)-induced chromosome aberrations was exacerbated by XRCC1 deficiency and the spectrum of chromosome damage changed dramatically. Specifically, chromatid and isochromatid lesions were the most prominent aberrations induced in the cell lines and XRCC1 was essential to reduce the formation of chromatid lesions. In addition, XRCC1 deficiency caused a dramatic increase in the number of chromatid exchanges indicating that it is involved in protection from Cr(VI)-induced chromosome instability.

Chromium Is Elevated in Fin Whale (Balaenoptera physalus) Skin Tissue and Is Genotoxic to Fin Whale Skin Cells.

Hexavalent chromium (Cr(VI)) is present in the marine environment and is a known carcinogen and reproductive toxicant. Cr(VI) is the form of chromium that is well absorbed through the cell membrane. It is also the most prevalent form in seawater. We measured the total Cr levels in skin biopsies obtained from healthy free-ranging fin whales from the Gulf of Maine and found elevated levels relative to marine mammals in other parts of the world. The levels in fin whale biopsies ranged from 1.71 to 19.6 µg/g with an average level of 10.07 µg/g. We also measured the cytotoxicity and genotoxicity of Cr(VI) in fin whale skin cells. We found that particulate and soluble Cr(VI) are both cytotoxic and genotoxic to fin whale skin cells in a concentration-dependent manner. The concentration range used in our cell culture studies used environmentally relevant concentrations based on the biopsy measurements. These data suggest that Cr(VI) may be a concern for whales in the Gulf of Maine.