Exposure to crude oil during spill events causes a variety of pathologic effects in birds, including oxidative injury to erythrocytes, which is characterized in some species by the formation of Heinz bodies and subsequent anemia. However, not all species appear to develop Heinz bodies or anemia when exposed to oil, and there are limited controlled experiments that use both light and electron microscopy to evaluate structural changes within erythrocytes following oil exposure. In this study, we orally dosed zebra finches (Taeniopygia guttata) with 3.3 or 10 mL/kg of artificially weathered Deepwater Horizon crude oil or 10 mL/kg of peanut oil (vehicle control) daily for 15 days. We found that birds receiving the highest dosage experienced a significant increase in reticulocyte percentage, mean corpuscular hemoglobin concentration, and liver mass, as well as inflammation of the gastrointestinal tract and lymphocyte proliferation in the spleen. However, we found no evidence of Heinz body formation based on both light and transmission electron microscopy. Although there was a tendency for packed cell volume and hemoglobin to decrease in birds from the high dose group compared to control and low dose groups, the changes were not statistically significant. Our results indicate that additional experimental dosing studies are needed to understand factors (e.g., dose- and species-specific sensitivity) and confounding variables (e.g., dispersants) that contribute to the presence and severity of anemia resulting from oil exposure in birds.

In early nineteen century, a gas field was operational in southern part of Sindh, Pakistan for power production. The plant was completely un-operational for last three decades, whereas all wastage and raw materials are still dumped there, which might be the source to contaminate the ground water. The most of the workers population still living in different villages nearby the gas field. In present study, evaluated the undesirable effects of the toxic metals (lead and cadmium) via consuming groundwater for drinking and other domestic purpose especially in children of ≤5.0 years. For comparative purpose groundwater of nonindustrial area (nonexposed) was also analysed and their impact on age matched children was carried out. Biological samples (scalp hair and blood) were collected from children of exposed and nonexposed areas. The Cd and Pb in scalp hair and blood samples were carried out by graphite furnace atomic absorption spectrometry. Whereas, Cd and Pb in groundwater obtained from both areas were determined prior to applied preconcentration method as reported in our previous works. The Cd and Pb contents in the groundwater of villages of exposed area were found in the range of 5.18–10.9 and 19.9–69.5 μg/L, respectively. Whereas, the groundwater of nonexposed area contains Cd and Pb in the range of 1.79–3.78 and 5.07–24.3 μg/L, respectively. It was observed that the concentrations of Cd and Pb in scalp hair and blood samples of children belongs to exposed area have ≥2.0 fold higher than the resulted data attained for age matched control children, indicating as the exposure biomarkers of toxic metals. The children belong to exposed area have poor health, anemic and low body mass index (<13 kg/m2). A significant positive correlations among Cd and Pb concentrations in biological samples of exposed subjects and groundwater was observed (p < 0.01).

A prospective cohort study of a Chinese population was conducted to investigate the relationship between prenatal phthalates exposure and maternal hemoglobin or anemia. Based on the Ma'anshan Birth Cohort study, 7 phthalate metabolites were quantified in spot pregnancy urine samples (n = 9263) from 3269 pregnant women during each trimester. The maternal hemoglobin concentrations were obtained from electronic medical records at the same three time points for each participant during pregnancy. Anemia was defined as a hemoglobin concentration below 110 g/L in pregnant women. Repeated measures and trimester-specific analyses were used to estimate the effects of phthalates exposure on maternal hemoglobin and anemia. The prevalence of anemia was 3.6%, 27.0%, and 26.5% during the first, second and third trimester, respectively. Repeated measures analysis showed that hemoglobin concentrations decreased by 0.55, 0.19, 0.57, 0.49, and 0.54 g/L with each 1 ln-transformed concentration increase of MBP, MBzP, MEHP, MEOHP, and MEHHP, respectively. Exposure to MMP, MBP, MEHP, MEOHP, and MEHHP increased the risk of anemia by 1.11-fold, 1.21-fold, 1.20-fold, 1.13-fold, and 1.16-fold, respectively. Trimester-specific regression models stratified by the sample collection time during pregnancy generated consistent results. This is the first study focusing on the effect of prenatal phthalate exposures on hemoglobin or anemia in pregnant Chinese women. We found that prenatal phthalates exposure not only decreased the concentrations of hemoglobin but also showed associations with the prevalence of anemia. Associations appeared stronger for the subsample representing women pregnant with a male fetus than those pregnant with a female fetus. Anemia remains a moderate public health problem in China, and effective measures should be implemented.

Among wild birds, lead (Pb) exposure caused by ingestion of ammunition is a worldwide problem. We aimed to reveal the behavior and toxic effect of Pb caused by ingesting Pb shots in waterfowl. Four male, eight-week old Muscovy ducks (Cairina moschata) were given three Pb shots (approximately 240 mg in total) orally and then fed for 29 days after exposure, simulating a low-dose Pb exposure in wild waterfowl. During the breeding period, blood samples were collected 10 times, and fecal samples every day. Additionally, 22 fresh tissue and 6 bone samples were obtained from each duck through the dissection. Although there were no gross abnormalities, the maximum blood Pb concentration of each duck ranged from 0.6 to 3.7 mg/L, reaching a threshold concentration indicative of clinical symptoms (>0.5 mg/L). δ-aminolevulinic acid dehydratase declined one day after exposure and remained low throughout the feeding period. Hematocrit also tended to decrease, indicating signs of anemia. The highest Pb accumulation was observed in the bones, followed by the kidneys, intestinal tracts, and liver. High Pb accumulation in the bones, which are known to have a long Pb half-life, suggested that Pb would remain in the body and possibly affect bird health beyond 28 days after exposure. Gene expression analysis showed a significant increase in the expression of the toll-like receptor-3 gene, which is involved in virus discrimination in the liver, suggesting a disruption of the immune system. Microbiota analyses showed a correlation between the blood Pb concentration and the abundances of Lachnospiraceae and Ruminococcaceae, suggesting that Pb affects lipid metabolism. These results provide fundamental data on Pb exposure in wild birds and a new perspective on the damage such exposure causes.

Microcystins (MCs) produced by cyanobacteria are potent toxins to humans that cannot be ignored. However, the toxicity of MCs to humans remains largely unknown. The study explored the role of MCs in the development of hematological parameters through human observations and a chronic mouse model to explore related mechanisms. The adjusted odds ratio of MC-LR to the risk of anemia was 4.954 (95 % CI, 2.423–10.131) in a case-control study in Nanjing. An inverse correlation between serum MC-LR and hemoglobin (HGB), hematocrit (HCT), mean corpuscular volume (MCV), and red blood cell count (RBC) was observed. MC-LR in the serum of the population was an independent risk factor for microcytic anemia. Animal experiments demonstrated that MC-LR resulted in microcytic anemia, which is associated with inflammation, dysregulation of iron homeostasis, and erythropoiesis. We first identified the possible signaling pathway of MC-LR-induced anemia that MC-LR significantly upregulated the levels of hepcidin via EPO/EPOR signaling pathway and the decreased levels of Twsg1 and Gdf15, thereby resulting in the decreased levels of Hbb and Fpn, and the increased expression of Fth1, and Tf in a chronic mouse model. Our study first identified that prolonged environmental exposure to MCs probably contribute to the occurrence of microcytic anemia in humans, which provides new insights into the toxicity of MCs for public health.

Data (N = 10644) for US adults aged ≥20 years for 2003–2016 from National Health and Nutrition Examination Survey were analyzed to evaluate the impact of co-occurrence of obesity with diabetes, anemia, albuminuria, and hypertension on concentrations of five perfluoroalkyl acids (PFAA), namely, perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS), perfluorodecanoic acid (PFDA), perfluorohexane sulfonic acid (PFHxS), and perfluorononanoic acid (PFNA). For the total population, males, and females, co-occurrence of obesity with hypertension, albuminuria, anemia, and diabetes was found to be associated with lower adjusted geometric means (AGM) than nonobese for every PFAA. For example for females, for PFOS, AGMs for obese with no diseases, hypertension, albuminuria, anemia, and diabetes were 8.2, 10.8, 5.8, 4.6, and 7.7 ng/mL respectively. In comparison, for PFOS, for nonobese females, AGMs for those with no diseases, hypertension, albuminuria, anemia, and diabetes were found to be 8.9, 13.4, 7.7, 6.0, and 10.2 ng/mL respectively. This implies obesity is associated with higher excretion rates. Females, in general, had lower AGMs than males for both obese and nonobese for every PFAA for every disease group. For example, percent ratios of obese females to males AGMs for PFOA were 66.7%, 87.1%, 88.2%, 70.6%, and 90% for those with no diseases, hypertension, albuminuria, anemia, and diabetes respectively. The ratios of obese to nonobese AGMs for females were lower than males for every PFAA for those with no diseases and hypertension only. For example, for PFOA for those with no diseases, obese to nonobese AGM ratios were 87% for females and 100% for males. Thus, additional excretion of certain PFAAs due to obesity is higher in females than males for those with no diseases and hypertension only.

Benzene exposure can cause pancytopenia and immunosuppression, leading to serious diseases such as aplastic anemia (AA) or acute myeloid leukemia (AML), but the underlying mechanism has not been fully elucidated. Hypoxia-inducible factor 1 (HIF-1) is an important transcription factor that regulates many downstream target genes. In this study, we reported a novel mechanism by which high expression of HIF-1α alleviated benzene toxicity. Mice with high expression of HIF-1α (HIF-1α⁺) were obtained by the Tet-on system and doxycycline induction, and they and wild-type (WT) mice were exposed to 150 mg/kg benzene for 0, 1, 3, 7, 10, 14, and 28 days. Dynamic changes in hematopoietic and immune-related indicators and the role of HIF-1α were explored. The level of white blood cells in mice reached the highest level on the third day, and immunity was activated and then suppressed within 10 days. Significant pancytopenia and immunosuppression occurred at 14 days and were more pronounced at 28 days. The levels of HIF-1α, EPO, VEGF, RORγt, and IL-17 in WT mice gradually decreased with increasing benzene exposure days, while the levels of Foxp3 and IL-10 increased. These changes were alleviated in HIF-1α⁺ mice. High expression of HIF-1α increased the levels of EPO and VEGF, which helped to maintain the stability of the hematopoietic microenvironment. Simultaneously, it attenuated benzene-induced immunosuppression by alleviating the Th17/Treg imbalance. HIF-1α is expected to be a new target for benzene-induced diseases such as AA and AML.

Data (N = 11251) from National Health and Nutrition Examination Survey (NHANES) for 2003–2016 for US adults aged ≥20 years were stratified by gender and anemia and analyzed to evaluate the associations between the concentrations of whole blood hemoglobin (WBHGB) and selected perfluoroalkyl acids (PFAAs) in serum by stages of glomerular filtration (GF). Investigated PFAAs were perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS), perfluorodecanoic acid (PFDA), perfluorohexane sulfonic acid (PFHxS), and perfluorononanoic acid (PFNA). Females with whole blood hemoglobin concentrations <12 g/dL and males with whole blood hemoglobin concentrations <13 g/dL were classified as being anemic. Regression models with log10 transformed concentrations of whole blood hemoglobin as dependent variable and age, poverty income ratio, body mass index, serum cotinine, daily alcohol intake, survey year, and log10 concentrations of one of the PFAA as independent variables were fitted. For anemic females, association between WBHGB and PFAA concentrations were uniformly positive across worsening stages of renal failure and percent increases for 10% increases in PFAAs varied between 0.03% and 0.39%. For anemic males, association between WBHGB and PFAA concentrations were positive except at GF-3A (45 ≤ eGFR<60 mL/min/1.73 m²) and percent increases for 10% increases in PFAAs varied between 0.02% and 0.53%. Thus, more often than not, presence of positive associations between WBHGB and PFAA among anemics imply elevated levels of PFAA are associated with higher levels of WBHGB. Similar results were observed for non-anemic males and females, however strengths of associations between whole blood hemoglobin and PFAAs were several fold higher among anemic compared to non-anemic participants. Hemoglobin is consistently associated with serum PFAAs.

Exposure to lead among children, as well as adults, is a major global health issue. With diverse routes of exposure (e.g., food, air, and water) either environmentally or occupationally, lead among children can cause mild, moderate, to severe health complications in the later stages of life. The average blood lead level reported by CDC in 2021 is 3.5 µg/dL, and the level of blood lead toxicity is ≥ 10 μg/dL. In this study, we planned to systematically analyze the association between blood lead levels (BLLs) (≥ 10 μg/dL and < 10 μg/dL) and the risk of anemia (hemoglobin level < 11 g/dL) among Indian children aged between ≥ 1 and ≤ 18 years. An online literature search of 5 databases, PubMed, Ovid, EMBASE, Web of Science, and Google Scholar was accomplished with a search updated until 8ᵗʰ March 2021. Study designs included cohort, cross-sectional, and case–control studies that have evaluated the association of lead toxicity or exposure with anemia (Hb < 11 g/dL) reported in urban and/or rural Indian children. Meta-analysis was performed among a total of 864 children from 4 cross-sectional studies. The association between lead toxicity (BLLs ≥ 10 μg/dL) and the risk of being anemic was not statistically significant (RR = 1.15 (95% CI: 0.86–1.55, I² = 77%). The risks of bias in all included studies were low according to the Newcastle Ottawa Scale. Increased blood lead levels did not appear to be the major contributor to anemia in Indian Children. We need to focus primarily on improving the nutritional quality, fortified food supplements, and a balanced diet for children to reduce the anemia burden in India. Lead toxicity should be sought as an etiological factor only in areas of high environmental risk factors which were leaded paints, leaded batteries, a house near major road/traffic areas, and pesticide exposure.

Fast growing arsenic menace is causing serious health hazards in Bihar, India, with an estimated 10 million people at risk. The exposed population is often unaware of the problem, which only amplifies the burden of arsenic health effects. In the present study, we have assessed the current situation of arsenic exposure in Chapar village of Samastipur district, Bihar. The health of the inhabitants was assessed and correlated with (1) arsenic concentrations in the groundwater of individual wells and (2) arsenic concentration found in their hair and urine. Altogether, 113 inhabitants were assessed, and 113 hair, urine and groundwater samples were collected. The health study reveals that the exposure to arsenic has caused serious health hazard amongst the exposed population with pronounced skin manifestations, loss of appetite, anaemia, constipation, diarrhoea, general body weakness, raised blood pressure, breathlessness, diabetes, mental disabilities, diabetes, lumps in the body and few cancer incidences. It was found that 52% of the total collected groundwater samples had arsenic levels higher than the WHO limit of 10 µg/l (with a maximum arsenic concentration of 1212 µg/l) and the reduced arsenite was the predominant form in samples tested for speciation (N = 19). In the case of hair samples, 29% of the samples had arsenic concentrations higher than the permissible limit of 0.2 mg/kg, with a maximum arsenic concentration of 46 µg/l, while in 20% exposed population, there was significant arsenic contamination in urine samples > 50 µg/l. In Chapar village, the probability of carcinogenic-related risk in the exposed population consuming arsenic contaminated water is 100% for children, 99.1% for females and 97.3% for male subjects. The assessment report shared to the government enabled the village population to receive two arsenic filter units. These units are currently operational and catering 250 households providing arsenic-free water through piped water scheme. This study therefore identified a significant solution for this arsenic-exposed population.