Cigarette smoke exposure is associated with the development and severity of chronic obstructive pulmonary disease, or COPD, which is the third leading cause of death worldwide.
Cigarette smoke contains 2–3 micrograms of cadmium, a highly toxic metal and environmental pollutant, per cigarette. Burning tobacco releases cadmium oxide that can be adsorbed onto microparticles in smoke that travel deep into the lungs. Furthermore, the body is not able to remove cadmium, which accumulates in longtime smokers.
In a Scientific Reportsstudy, University of Alabama at Birmingham researchers show how a low dose of cadmium produces a deleterious stress in lung epithelial cells, and their findings highlight potential therapeutic targets to be explored in cadmium-exposure and subsequent lung injury.
The research, led by Veena Antony, M.D., a professor in the UAB Department of Medicine, focuses on microRNA-381, and the expression of a chloride channel gene called ANO1 in lung tissue samples and airway epithelial cells. ANO1 helps produce mucus in the airway; but overproduction of mucus in chronic lung disease can lead to airway thickening and mucus blockage, adding to severity of the disease. Thus, overexpression of ANO1 can exacerbate COPD.
The UAB researchers compared lung tissue samples from nine “never” smokers, who had zero history of cigarette smoking, and lung tissue samples from 13 “ever” smokers with COPD who had a history of smoking that ranged from 15 to 25 pack years per person.
One pack year is generally defined as smoking one pack of cigarettes a day for one year. The researchers found that “ever” smokers, in contrast to “never” smokers, had upregulated ANO1 expression in airway epithelial cells.
Similarly, airway epithelial cells in a bronchoalveolar lavage fluid from one non-COPD subject and one smoker with COPD showed greater ANO1 expression in the COPD-subject cells.
The researchers next tested the direct effect of very low doses of cadmium on normal human airway epithelial cells. These cells were grown on an air-liquid interface that allows the airway cells to differentiate normally. Two weeks of exposure to 0.5 or 1.0 micromolar cadmium chloride in the liquid layer increased expression of ANO1 12 to 14 times.
MicroRNAs have the ability to downregulate expression of a gene by direct interaction with that gene’s mRNA sequence. The UAB team used computer software analysis to identify microRNA-381 as the microRNA with most interaction with ANO1 mRNAs, suggesting that microRNA-381 is a negative regulator of ANO1. Some heavy metals are known to negatively regulate microRNAs.
Antony and colleagues used a synthetic inhibitor for microRNA-381 to inhibit the expression of microRNA-381 in primary human airway epithelial cells from subjects with COPD, and found that ANO1 expression was upregulated significantly.
To study the association between maternal exposure to arsenic, cadmium, lead, manganese and mercury, time-to-pregnancy (TTP) and infertility.
Design
Pregnancy-based retrospective TTP cohort study.
Setting
Hospitals and clinics from ten cities across Canada.
Population
A total of 1784 pregnant women.
Methods
Concentrations of arsenic, cadmium, lead, manganese and mercury were measured in maternal whole blood during the first trimester of pregnancy as a proxy of preconception exposure. Discrete-time Cox proportional hazards models generated fecundability odds ratios (FOR) for the association between metals and TTP. Logistic regression generated odds ratios (OR) for the association between metals and infertility. Models were adjusted for maternal age, pre-pregnancy body mass index, education, income, recruitment site and plasma lipids.
Main Outcome Measures
TTP was self-reported as the number of months of unprotected intercourse to become pregnant. Infertility was defined as TTP longer than 12 months.
Results
A total of 1784 women were eligible for the analysis. Mean ± SD maternal age and gestational age at interview were 32.2 ± 5.0 years, and 11.6 ± 1.6 weeks, respectively. Exposure to arsenic, cadmium, manganese or mercury was not associated with TTP or infertility. Increments of one standard deviation of lead concentrations resulted in a shorter TTP (adjusted FOR 1.09, 95% CI 1.02–1.16); however, the association was not linear when exposure was modelled in tertiles.
Conclusion
Blood concentrations of metals at typical levels of exposure among Canadian pregnant women were not associated with TTP or infertility. Further studies are needed to assess the role of lead, if any, on TTP.
1 INTRODUCTION
Environmental exposure to metals is a public health concern given their wide dispersion in the environment and potential endocrine disruptive properties.1–3 An endocrine endpoint of interest in reproductive and environmental epidemiology is human fecundity given the increased rates of gynaecological conditions associated with impaired fecundity and possible association with exposure to endocrine-disrupting chemicals.4–7 There is evidence linking metals like arsenic, cadmium, lead and mercury to impaired ovarian function through oxidative stress.1, 2 In contrast, other metals like manganese, an essential trace element, may prevent oocyte damage through antioxidant properties.8–10
Although several environmental chemicals have been associated with decreased fecundability or a longer time-to-pregnancy (TTP),11–15 the impact of metals on TTP and infertility needs further investigation. The effect of lead is of particular interest, given its high toxicity at high levels of exposure in almost every organ. At current environmental levels of exposure, the most notable and strongest association observed with lead exposure is its detrimental effect on children’s neurological function.16, 17 The existing body of research exploring the relationship between female fecundity and lead exposure is limited, and the findings are inconclusive.18–21 Further investigation is warranted to provide a clearer understanding of a potential association.
Two previous cohort studies have investigated the effect of metals on TTP. The New York Angler Cohort, a prospective cohort study including 80 women, reported that higher pre-pregnancy levels of magnesium were associated with a shorter TTP and zinc exposure was associated with a longer TTP, but there was no association for arsenic, cadmium or lead.20 The Longitudinal Investigation of Fertility and the Environment (LIFE) study assessed the effects of environmental chemicals and human fecundity among 501 couples in Michigan and Texas.21 Male lead and female cadmium concentrations were associated with reduced fecundability. When jointly modelling couples’ exposures, only male lead concentration significantly reduced fecundability.21 The few studies that have assessed the impact of environmental metals exposure on infertility (i.e. inability to conceive after 12 months of unprotected intercourse) have reported associations with infertility at increased levels of cadmium or lead.22–24
This study aims to evaluate the association between selected metals (arsenic, cadmium, lead, manganese and mercury), TTP and infertility in participants from the Maternal–Infant Research on Environmental Chemicals (MIREC) study, a Canadian pregnancy and birth cohort.
RESULTS
A total of 1784 participants from the MIREC study met our eligibility criteria (Figure 1). The distribution of demographic and lifestyle characteristics of the study population and their association with TTP are presented in Table 1. Mean maternal age at interview was 32.2 ± 5.0 years and mean gestational age at the time of the blood sample was 11.6 ± 1.6 weeks (± SD). Participants in this study were mostly White, born in Canada, lifelong non cigarette smokers and had a normal pre-pregnancy BMI. Almost two-thirds had an undergraduate degree or higher, more than one-third reported a household income greater than Can$ 100 000, and over half had one previous pregnancy with a live birth.
TABLE 1. Characteristics of 1784 women from the MIREC study, 2008–2011, and association with time-to-pregnancy.
n (%)
Time-to-pregnancy (months)
Crude FOR (95% CI)
Mean ± SD
Median (IQR)
Maternal age (years)
≤29
524 (29.4)
3.8 ± 6.9
1 (1–4)
1.00
30–34
650 (36.4)
4.6 ± 7.4
2 (1–4)
0.81 (0.70–0.94)
35+
610 (34.2)
7.0 ± 12.8
2 (1–6)
0.62 (0.54–0.72)
Pre-pregnancy BMI (kg/m2)
<24.9
1052 (59.0)
4.8 ± 8.6
1 (1–4)
1.00
25–29.9
362 (20.3)
5.2 ± 10.7
1 (1–4)
1.03 (0.89–1.21)
>30
245 (13.7)
6.6 ± 11.1
1 (1–7)
0.76 (0.64–0.91)
Missing
125 (7.0)
5.2 ± 10.6
1 (1–4)
1.03 (0.82–1.31)
Education
Some college or less
281 (15.8)
5.1 ± 9.8
1 (1–5)
1.00
College diploma
378 (21.2)
5.7 ± 10.2
2 (1–6)
0.88 (0.73–1.08)
Undergraduate
655 (36.7)
5.5 ± 10.8
2 (1–5)
0.96 (0.81–1.15)
Graduate (MSc, PhD)
470 (26.3)
4.4 ± 6.6
2 (1–4)
1.02 (0.84–1.23)
Income (Can$)
<Can$ 60 000
374 (21.0)
4.0 ± 6.9
1 (1–4)
1.00
Can$ 60 001–Can $ 100 000
624 (35.0)
5.4 ± 10.1
2 (1–5)
0.81 (0.69–0.96)
>Can$ 100 000
702 (39.3)
5.6 ± 10.2
2 (1–5)
0.77 (0.66–0.91)
Missing
84 (4.7)
5.0 ± 10.7
2 (1–4)
0.90 (0.66–1.22)
Country of birth
Foreign
336 (18.8)
5.0 ± 8.0
2 (1–6)
1.00
Canada
1448 (81.2)
5.2 ± 9.9
2 (1–5)
1.04 (0.90–1.21)
Race and ethnicity
White
1487 (83.4)
5.1 ± 9.7
2 (1–5)
1.00
Not White
297 (16.6)
5.4 ± 8.9
2 (1–6)
0.93 (0.79–1.08)
Maternal cigarette smoking
Never
1087 (60.9)
5.1 ± 8.8
2 (1–5)
1.00
Former
491 (27.5)
5.3 ± 10.8
2 (1–4)
1.06 (0.92–1.21)
Current
206 (11.5)
5.1 ± 10.2
2 (1–4)
1.09 (0.90–1.32)
Parity
Nulliparous
850 (47.6)
6.1 ± 11.3
2 (1–6)
1.00
Parous
934 (52.4)
4.4 ± 7.6
2 (1–4)
1.19 (1.06–1.34)
Total plasma lipids (g/L)
<5.60
537 (30.1)
4.2 ± 7.8
2 (1–4)
1.00
5.60–6.60
613 (34.4)
5.0 ± 8.9
2 (1–5)
0.86 (0.74–1.00)
>6.60
619 (34.7)
6.2 ± 11.4
2 (1–6)
0.75 (0.65–0.87)
Missing
15 (0.8)
6.5 ± 9.7
2 (1–6)
0.62 (0.32–1.20)
Abbreviations: BMI, body mass index; CI, confidence interval; FOR, fecundity odds ratio; IQR, interquartile range; SD, standard deviation.
The cumulative conception rate was 44.8% at 1 month, 81.9% at 6 months and 90.8% at 12 months. Hence, the rate of infertility (TTP > 12 months) in this cohort was 9.2%. Maternal age, pre-pregnancy BMI, income, parity and total plasma lipids were associated with TTP (Table 1). Older women, with higher BMI, higher income or increased plasma lipids had decreased fecundability (longer TTP). Parous women had a shorter TTP. Education, country of birth, race and ethnicity, and cigarette smoking status were not associated with TTP (Table 1).
Most participants had detectable blood levels of all five metals (Table 2). Geometric means for arsenic, cadmium, lead, manganese and mercury were 0.73 μg/L, 0.21 μg/L, 0.62 μg/dL, 8.79 μg/L and 0.61 μg/L, respectively. TABLE 2. Whole blood concentrations of metals, MIREC study 2008–2011.
In relation to TTP, increments of one SD increase in blood concentrations of arsenic, cadmium, manganese or mercury were not associated with TTP (Table 3). In the adjusted model, increments of one SD of lead concentrations resulted in a shorter TTP (adjusted FOR [aFOR] 1.09; 95% CI 1.02–1.16). When exposure was modelled as tertiles, no relationship was observed between arsenic, cadmium, manganese or mercury and TTP. For lead, relative to the first tertile, the second (aFOR 1.33; 95% CI 1.14–1.54) and third (aFOR 1.28; 95% CI 1.10–1.50) tertiles were associated with a shorter TTP (Table 3). TABLE 3. Fecundability odds ratios for the association between metals and time-to-pregnancy, MIREC study 2008–2011.
Note: FOR derived from Cox proportional hazards model modified for discrete time data with multiple imputation (m = 20) for missing covariate information.
Abbreviations: CI, confidence interval; FOR, fecundity odds ratio.
a Adjusted for maternal age, pre-pregnancy body mass index, education, income, country of birth, race and ethnicity, maternal cigarette smoking, plasma lipids and recruitment site.
In relation to infertility (TTP > 12 months), increments of one SD increase of blood concentrations of arsenic, cadmium, lead, manganese or mercury were not associated with infertility (Table 4). When modelled as tertiles, exposures to arsenic, cadmium or mercury were not associated with infertility. For lead, relative to the first tertile, the second tertile was associated with decreased odds of infertility (aOR 0.57; 95% CI 0.37–0.87), but not the third tertile (Table 4). For manganese, relative to the first tertile, no association was observed with the second tertile, but the third tertile was associated with decreased odds of infertility (aOR 0.64; 95% CI 0.42–0.96) (Table 4). TABLE 4. Odds ratios for the association between blood metals and infertility, MIREC study 2008–2011.
a Adjusted for maternal age, pre-pregnancy body mass index, education, income, country of birth, race and ethnicity, maternal cigarette smoking, plasma lipids and recruitment site.
In the sensitivity analysis stratified by parity (Table S1), the association between lead and shorter TTP remained among nulliparous (aFOR 1.10; 95% CI 1.01–1.21), and parous (aFOR 1.09; 95% CI 1.00–1.19) women. When including parity in the adjusted model (Table S2), results were similar to the main analysis presented in Table 3. The sensitivity analysis stratified by manganese levels yielded similar results in terms of FOR, except for lead where a slight attenuation in the 95% CI occurred in those with manganese concentration above the median (Table S3).
4 DISCUSSION
4.1 Main findings
In this pregnancy-based retrospective TTP cohort study in participants from the Canadian MIREC study, environmental exposure to arsenic, cadmium, manganese and mercury measured during the first trimester were not associated with TTP or infertility. Exposure to lead was associated with a shorter TTP, but the pattern of effect was not consistent with a dose–response relationship.
4.2 Strengths and limitations
The major strengths of this study include its large sample size and the use of biomarkers as an objective measure of total metal exposure. The limitations of this research are related to the retrospective assessment of exposure and outcome, residual confounding and an underlying cohort of women who became pregnant, and therefore excluded those with infertility who did not access fertility treatment or were not successful after treatment.
The measurement of exposure was taken during the first trimester of pregnancy as a proxy for pre-conception exposure. The accuracy of this measure is impacted by the stability of participant’s behaviour in relation to metal exposures, and by physiological changes during pregnancy. Both sources of error would contribute to non-differential exposure measurement error in this study and would tend to bias effect estimates towards the null, given that the measurement of exposure was collected during the first trimester of pregnancy in all participants independent of TTP. Furthermore, most of the metals included have a relatively long half-life (3–4 months for cadmium,34 90 days for lead,35 2–5 weeks for manganese36–38 and 44–80 days for mercury39–41), except for arsenic, which has a half-life of only several hours.42 However, with continuous exposure, concentrations may reach a steady state.33 Concerning the outcome, TTP was collected by questionnaire and relies on subject recall. However, the collection of retrospective TTP is a reliable method when data are collected in the short term, as was the case in the MIREC study.43
There is also the potential for residual confounding, due to the unavailability of some data in the MIREC study, such as menstrual cycle regularity, associated gynaecological conditions and coital frequency. The absence of sociodemographic and biomonitoring data for the male partner in the MIREC study is another limitation. For example, the LIFE study reported that male partners’ metal concentrations were more often associated with reduced couple fecundability compared with female partners’ concentrations.44
In addition, the study population was restricted to women who have had a birth and/or became pregnant, inherently conditioning on fertility. This introduces the potential for collider bias, which occurs when exposure and outcome each influence a common third variable, and that variable is conditioned on in the design or analysis.45 In the MIREC study, participants are restricted to those who have had a birth. Both the exposure (lead) and outcome influence fertility status and could therefore produce a collider bias because the study population has been restricted to those able to conceive.46, 47 However, biologically, there is a wide range of reproductive capacity, even among couples who achieve pregnancy. This heterogeneity is expressed in the gradual decrease in conception rates during successive months of trying,47, 48 which is not a true time effect, but evidence of sorting among individuals who are heterogeneous in their capacity to conceive.48 Heterogeneity among couples raises the possibility that some of this variation may be explained by identifiable factors, supporting the rationale of our study. Finally, as the MIREC cohort consists mainly of healthy mothers of moderate to high socioeconomic status, and Caucasian race and ethnicity,25 metal concentrations and other factors associated with TTP might differ from other populations, limiting the external generalisability of our results.49
4.3 Interpretation
Two studies have evaluated the relationship between metals and TTP, and both were prospective cohort studies of pre-conception couples. The LIFE Study observed a reduction in couple fecundity with higher exposure to cadmium and lead. When assessing individual partner exposure, female cadmium exposure (aFOR 0.78, 95% CI 0.63–0.97) and male lead exposure (aFOR 0.85, 95% CI 0.73–0.98) were associated with a longer TTP. No association was observed with mercury. Except for mercury, geometric mean concentrations of blood metals in MIREC participants (0.21 μg/L for cadmium, 0.62 μg/dL for lead and 0.61 μg/L for mercury) were similar to those reported in the LIFE study (0.21 μg/L for cadmium, 0.66 μg/dL for lead and 0.98 μg/L for mercury).21 The prospective design of the LIFE study, and the difference in sociodemographic characteristics compared with the MIREC study could explain the differences in our results. On the other hand, consistent with our results, the prospective cohort study using preconception enrolment of women from the New York Angler Cohort did not find evidence to support the association between low-level exposure to toxic metals and fecundity, even though the concentrations of metals in the Angler Cohort were higher than in MIREC (4.27 μg/L for arsenic, 1.63 μg/L for cadmium, 1.55 μg/dL for lead).20 However, the small number of participants included in this cohort (n = 80) may have made it underpowered to detect any association.
We remain uncertain about the observed association between lead exposure and a shorter TTP. To our knowledge, no other study has reported a similar finding. The absence of a dose–response when the exposure is modelled as tertiles or restricted cubic splines, suggests a spurious association, which could be a result of the above-mentioned limitations of our study. To further explore this association, we investigated the potential impact of gestational age at the time of sample collection on the association between lead exposure and TTP. This exploration was motivated by the understanding that blood lead concentrations encompass both ongoing exposure and lead stores in bone.50 During pregnancy, heightened calcium demands induce increased bone turnover, leading to the release of lead from bone and subsequent increase in blood lead levels.50–52 Our hypothesis posited a reduced fecundability (longer TTP) for metals in women’s samples collected after 10 weeks of gestation. However, we were not able to demonstrate this, as lead continued to be associated with a shorter TTP independent from the gestational age at the time of interview.
Regarding infertility, authors of an analysis among 124 participants of the 2013–2014 and 2015–2016 National Health and Nutrition Examination Surveys (NHANES) reported an association between log-transformed blood lead (OR 2.60, 95% CI 1.05–6.41) and cadmium (OR 1.84, 95% CI 1.07–3.15) and self-reported infertility.22 The geometric mean of blood lead was lower in this study (0.50 μg/dL) compared with MIREC; however, the geometric mean of blood cadmium (0.26 μg/L) was similar. Another study including a larger sample of 838 participants from the 2013–2018 NHANES reported no association between blood concentrations of cadmium or mercury and self-reported infertility.23 Lead concentrations were associated with infertility in some categories but with no overall dose–response pattern.23 Compared with MIREC, mean concentrations of cadmium and mercury in NHANES were higher (0.45 μg/L for cadmium, 1.15 μg/L for mercury); however, concentrations of lead were the same (0.70 μg/dL). We found a decreased odds of infertility in the second tertile (0.50–0.77 μg/dL) of exposure for lead (OR 0.52, 95% CI 0.33–0.84), but not in those in the highest tertile (>0.77 μg/dL) or when the exposure was modelled as a continuous variable.
5 CONCLUSION
Our study supports the theory that at current environmental levels of exposure, which are low relative to levels seen in other populations, metals are not associated with decreased fecundability or infertility. Further studies are needed to assess the role of lead, if any, on TTP and infertility.
Two new studies on dietary exposure to heavy metals clarify their connections to cancers and other serious illnesses.
WASHINGTON, DC, 2023, December 12, 2023 – The problem of foodborne metal contamination has taken on new urgency, thanks in part to a 2021 US Congressional Report detailing high levels of metals found in infant food pulled off grocery shelves. (More recently, high levels of lead were discovered in children’s fruit puree pouches.) Now, two new studies provide information on the correlation between exposure to heavy metals in food and the risk of cancers and other serious health risks. The findings will be presented at the 2023 Society for Risk Analysis Annual Conference. Food crops can absorb heavy metals from contaminated soil, air, and water. As a result, traces of dangerous heavy metals – lead, arsenic, and cadmium – are found in common foods from rice and cereals to nuts and spinach. Felicia Wu, Michigan State University food scientist and incoming president of the SRA, is leading several investigations to gain a better understanding of the health risks of heavy metal exposure. She will present the results of two recent studies at the December SRA meeting. The first is a comprehensive evaluation of the health risks associated with dietary exposure to lead, arsenic, and cadmium. The second is a quantitative assessment of the risk of cancer from inorganic arsenic exposure. “Results from these studies have important implications for food safety regulations, public health policies, and consumer awareness” says Wu. Health risks of dietary exposure to lead, arsenic, and cadmium In the first study, Wu, working with postdoctoral research fellow Charitha Gamlath and Ph.D. student Patricia Hsu, gathered data on the dietary intake of each metal from various sources such as food and water samples and existing studies and reports. The researchers analyzed the data to determine the strength of the association between dietary exposure and adverse health effects. Both cancer and non-cancer health effects were considered, and the strengths of the links between heavy metal exposure and each effect using Bradford Hill Criteria scores. Lead is a toxic metal commonly found in old paint, water pipes, and contaminated soil. Food sources of lead include root vegetables like beets. In the study, lead showed moderate to high risk scores for causing lung, kidney, bladder, stomach, and brain cancers. It also showed moderate to high scores for non-cancer risks (hematopoietic, reproductive, neurological, renal, and respiratory effects).
Arsenic is a naturally occurring toxic element that can contaminate drinking water and food – especially in areas with high levels of arsenic in the soil. It can be found in rice, wheat, and leafy green vegetables, among other foods. Arsenic demonstrated moderate to high scores for skin, bladder, lung, kidney, and liver cancers. It also showed moderate to high scores for non-cancer risks (skin lesions, cardiovascular disease, immunological, neurological, reproductive, developmental, and renal effects). Cadmium is a toxic metal found in nuts, potatoes, seeds, cereal grains, leafy green vegetables, and tobacco smoke. Among its sources in the environment are fertilizers and industrial emissions. In the study, cadmium revealed moderate to high risk scores for prostate, renal, bladder, breast, pancreatic, and endometrial cancers. It also showed moderate to high scores for non-cancer risks (renal, developmental, reproductive, immunological, and neurological effects). Earlier this year, Wu co-authored a study on cadmium in baby food that was published in Food and Chemical Toxicology. In that paper, the researchers found that babies and young children 6 months to 5 years old are the most highly exposed to cadmium in common foodstuffs. American infants and young children of these age groups who regularly consumed rice, spinach, oats, barley, potatoes, and wheat had mean cadmium exposures exceeding the maximum tolerable intake level set by the Agency for Toxic Substances and Disease Registry (ATSDR). Arsenic exposure and bladder, lung, and skin cancer cases in the U.S. In the second study to be presented, Wu and Ph.D. student Rubait Rahman conducted a quantitative cancer risk assessment for different food products in the United States containing inorganic arsenic. Their preliminary estimates suggest that every year, more than 6,000 additional cases of bladder and lung cancers and over 7,000 cases of skin cancers can be attributed to the consumption of inorganic arsenic in the United States. The researchers also found that certain food products can be associated with higher cancer risk than others. These include rice, wheat, and leafy green vegetables. For this project, a comprehensive review of scientific literature was conducted to identify relevant studies on inorganic arsenic contamination in various food products and associated cancer risks. Data on arsenic levels in food products were obtained from regulatory agencies, such as the U.S. Food and Drug Administration (FDA) and the U.S. Department of Agriculture (USDA). Quantitative cancer risk assessment models were applied to estimate the cancer risk attributable to inorganic arsenic exposure through different food products. These models integrated exposure data, dose-response relationships, and population characteristics to quantify the probability of cancer occurrence.
It’s unsettling to realize that the U.S. Food and Drug Administration (FDA) permits trace amounts of insects, rodent hair, and feces in our food supply. Equally alarming is the revelation that federal regulations allow food producers to incorporate heavy metals into our meals.
Recent research draws attention to the dangerous levels of heavy metals in food, posing exceptionally high risks to children. Both this study and another investigation confirm that ingesting these heavy metals through food can lead to cancer and other severe health complications.
From baby spoons to big plates: How heavy metals contaminate our food supply
The issue of metal contamination in our food is deeply concerning, with a spotlight on its presence in baby food drawing heightened attention from health experts. Just a couple of years ago, a U.S. Congressional Report exposed alarming levels of metals in baby food, prompting their removal from store shelves. More recently, similar levels of concern have been detected in fruit purees targeted at children.
The studies above shed light on the concerning connection between heavy metal exposure through infant food consumption and increased cancer risk.
So, how do these heavy metals infiltrate our food chain? Crops can absorb these contaminants from polluted groundwater, tainted soil, and airborne particles. Detailed examinations of food components have unveiled trace amounts of toxic heavy metals like cadmium, arsenic, and lead, not only in baby food but also in certain adult food products.
Cadmium in crops: Silent threat lurking in our favorite foods
The heavy metal cadmium seeps into produce through emissions from factories and fertilizers. Cadmium is toxic, yet trace amounts are commonly found in the following foods:
Leafy green veggies
Grain used in cereal
Potatoes
Nuts
Cadmium toxicity causes a moderate-to-high risk for endometrial, pancreatic, bladder, breast, and prostate cancer. The same elevated risk level holds true for non-cancer health issues such as neurological, immunological, and reproductive problems.
It is the most vulnerable among us who are likely to consume cadmium. Researchers determined babies and youngsters between six months and five years of age are exposed to this heavy metal more frequently than other age cohorts.
American babies and youngsters who consume wheat, oats, spinach, rice, and potatoes surpass the maximum acceptable intake amounts established by the Agency for Toxic Substances and Disease Registry (ATSDR), a federal public health agency created to help reduce the human health risks caused by exposure to harmful substances.
Heavy metals are also present in a wide variety of adult foods
While the medical community is chiefly alarmed by the presence of detrimental heavy metals in infant foods, it’s crucial to recognize that adults are not exempt from this risk. Heavy metals can be detected in various foods, from spinach to rice. Prolonged exposure to these contaminants, especially inorganic arsenic, is believed to play a role in the development of cancer.
The study linked above reveals the presence of lead in foods such as beets and other root vegetables spurs a moderate-to-high risk for the following cancers:
Brain
Lung
Bladder
Kidney
Stomach
The analysis also revealed the same moderate-to-high scores for risks aside from cancer, ranging from respiratory issues to reproductive problems, neurological challenges, and poor renal health.
Simple ways to reduce your heavy metal exposure
In an era of rising concerns about heavy metal exposure, taking proactive steps to safeguard your health is paramount. Here are some straightforward strategies to minimize your intake of these harmful contaminants:
Avoid processed foods: The foremost step to shield yourself from the threats of heavy metals is to eliminate processed foods from your diet. If you’re looking to feed your family healthy foods … buy organic ingredients and make the food yourself.
Opt for organic: Replace processed items with organic fruits and vegetables. Seek out produce from local farmers’ markets or the organic section of your nearby grocery store. Foods rich in fiber, such as bran, grains, and certain fruits, can help reduce the absorption of heavy metals in the body.
Use a sauna: Consider incorporating sessions in a far infrared sauna – several times per week. The sweat generated inside a sauna will help you to remove heavy metals plus many other unwanted toxins.
Stay hydrated: Even if you’re not consuming processed foods, consider boosting your hydration levels. Water aids in flushing out toxins from the body. Aim to drink an 8 oz glass of water every waking hour or two to promote detoxification.
Consumer Reports found dangerous heavy metals in chocolate from Hershey’s, Theo, Trader Joe’s and other popular brands. Here are the ones that had the most, and some that are safer.
December 15, 2022
By Kevin Loria
Data visualizations by Andy Bergmann
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For many of us, chocolate is more than just a tasty treat. It’s a mood lifter, an energy booster, a reward after a tough day, a favorite holiday gift.
People also choose dark chocolate in particular for its potential health benefits, thanks to studies that suggest its rich supply of antioxidants may improve heart health and other conditions, and for its relatively low levels of sugar. In fact, more than half of people in a recent survey from the National Confectioners Association described dark chocolate as a “better for you” candy.
But there’s a dark side to this “healthier” chocolate. Research has found that some dark chocolate bars contain cadmium and lead—two heavy metals linked to a host of health problems in children and adults.
The chocolate industry has been grappling with ways to lower those levels. To see how much of a risk these favorite treats pose, Consumer Reports scientists recently measured the amount of heavy metals in 28 dark chocolate bars. They detected cadmium and lead in all of them.
Heavy Metals in Dark Chocolate
CR tested a mix of brands, including smaller ones, such as Alter Eco and Mast, and more familiar ones, like Dove and Ghirardelli.
For 23 of the bars, eating just an ounce a day would put an adult over a level that public health authorities and CR’s experts say may be harmful for at least one of those heavy metals. Five of the bars were above those levels for both cadmium and lead.
That’s risky stuff: Consistent, long-term exposure to even small amounts of heavy metals can lead to a variety of health problems. The danger is greatest for pregnant people and young children because the metals can cause developmental problems, affect brain development, and lead to lower IQ, says Tunde Akinleye, the CR food safety researcher who led this testing project.
“But there are risks for people of any age,” he says. Frequent exposure to lead in adults, for example, can lead to nervous system problems, hypertension, immune system suppression, kidney damage, and reproductive issues. While most people don’t eat chocolate every day, 15 percent do, according to the market research firm Mintel. Even if you aren’t a frequent consumer of chocolate, lead and cadmium can still be a concern. It can be found in many other foods—such as sweet potatoes, spinach, and carrots—and small amounts from multiple sources can add up to dangerous levels. That’s why it’s important to limit exposure when you can.
Still, you don’t need to swear off chocolate entirely, Akinleye says. He adds that while most of the chocolate bars in CR’s tests had concerning levels of lead, cadmium, or both, five of them were relatively low in both. “That shows it’s possible for companies to make products with lower amounts of heavy metals—and for consumers to find safer products that they enjoy,” he says.
And in addition to choosing your dark chocolates wisely, there are a number of other steps you can take to continue enjoying chocolate safely.
We normally try our best on a day-to-day basis to make sound food choices and live a clean lifestyle. But sometimes an edible that we think encourages health can actually cause harm. Due to an affinity with heavy metals in the environment, some plants and animals absorb toxins like cadmium more readily than others. In light of this, steering clear of these common foods can help prevent serious problems down the road.
Hidden dangers
Over the last decade, flax has been embraced as an exceptionally healthy food, since it supplies ample amounts of omega-3 fatty acids, along with notable levels of lignins and fiber. Women wishing to avoid breast cancer have eagerly included the seed in their diet after learning about the protective phytoestrogens that flax supplies. However, researchers have discovered that flax also introduces cadmium into the body — which is notorious for encouraging breast cancer, kidney disorders, heart disease and osteoporosis. The soluble fiber of flax increases cadmium absorption, while the crop itself is known to take up cadmium from the soil, thereby infusing the plant with the metal.
Flax grown in heavily contaminated soil poses the greatest threat. Parts of Canada, where a majority of the world’s flaxseed is grown, tend to have high cadmium in the soil. North and South Dakota, two other large flax producers, also have soil with elevated levels. And flaxseed from China and India — two countries infamous for heavy metal pollution — are more likely than not to be contaminated. Since organic (as well as conventional) food isn’t tested for heavy metals by the USDA, the certified organic label is worthless in regard to cadmium found in flax. You can learn more about this state of affairs here.
Regrettably, flax isn’t the only edible at risk. Shellfish frequently contains cadmium as the result of environmental pollution. Inexpensive shrimp from Asia is one of the worst examples. Oysters from the east and west coasts of Canada are problematic too. Sunflower plants are also prone to accumulating cadmium. Beware of oil and seed butters made from sunflower, especially those grown in North and South Dakota. Polluted Louisiana is one of the main growing regions for rice in the United States, which is yet another crop that easily absorbs the metal. Additionally, if you are a fan of dried apricots, try to source varieties other than those grown in Turkey, which are often loaded with cadmium. Moreover, free-range escargot snails test high due to contaminated soil. Indian black mustard can also be troublesome.
ARYAN'S BLOG 