E-waste environmental contamination and harm to public health in China

Xu, Xijin; Zeng, Xiang; Boezen, H. Marike; Huo, Xia

doi:10.1007/s11684-015-0391-1

Cited by 77 publications

(19 citation statements)

References 51 publications

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“…Although they show less acute poisoning, the accumulation of these toxics inside would largely affect the health. Our results show that e-waste exposure would affect male reproductive health, which is consistent with other studies [20,21]. Although there are different views on whether or not the semen quality is decreasing, the environmental pollution is commonly accepted as the main critical influence factor [22,23].…”

Section: Discussionsupporting

confidence: 92%

The Impact of E-waste Occupational Exposure on Male Reproductive Health

Zhihai¹

2016

AJHR

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Electrical and electronic waste (e-waste) contains multiple toxic materials. However, there is currently a lack of exposure data on workers in formal recycling plants. This study aims to observe the influence of electronic waste (e-waste) on male's reproductive health and to provide a theoretical foundation for improving the occupational safety. A survey and sample collections were performed based on 210 workers in e-waste recycling plant as the exposure group and 210 residents who worked at the same area but not exposed to e-waste (other jobs) as the control group. Semen sperm analysis and TUNEL assay were applied to detect the apoptotic rate and single comet assay to detect DNA damage. The survey results showed that infertility rate of e-waste recycling workers was significantly higher than that of non-occupationally exposed workers (P < 0.05); e-waste occupationally exposed workers showed markedly higher rate of prostatitis, urethritis, abortion and preterm birth of their spouses (P < 0.05). The percentage of sperm concentration, motile sperm, 'a' level sperm, 'a+b' level sperm and live sperm of the exposure group were higher than control group (P < 0.05). TUNEL assay revealed that the apoptotic rate of sperms in the exposure group was higher too (P < 0.05). Further, the sperm comet length, tail length, tail DNA %, Olive tail moment were significantly different between the two groups (P < 0.05). In general, we concluded that occupational exposure to e-waste led to asthenospermia and increased male infertility. Occupational exposure to e-waste increased the sperm apoptosis rate and sperm DNA damage.

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Section: Discussionsupporting

confidence: 92%

The Impact of E-waste Occupational Exposure on Male Reproductive Health

Zhihai¹

2016

AJHR

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“…[15]. Mercury (Hg) exposure may lead to memory loss, immune toxicity, and muscle weakness [16]. Meanwhile, nickel (Ni) might contribute to dermatitis and bronchial asthma [17].…”

Section: Introductionmentioning

confidence: 99%

“…Meanwhile, nickel (Ni) might contribute to dermatitis and bronchial asthma [17]. In addition, persistent halogenated compounds such as brominated flame retardants can interfere with hormone function and cause neurobehavioral effects, behavioral disorders, and cancer [16,18,19]. E-waste workers are at risk from direct exposure to toxic substances during work, whereas others may be exposed to toxic substances contaminating the environment.…”

Section: Introductionmentioning

confidence: 99%

Exposure to Heavy Metals in Electronic Waste Recycling in Thailand

Kuntawee,

Tantrakarnapa,

Limpanont

et al. 2020

IJERPH

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Electronic waste recycling can release heavy metals into the environment and cause adverse health effects. We assessed the association between exposure to heavy metals from electronic waste recycling and the prevalence of asthma in a nested case-control study of 51 subject pairs with and without asthma. House dust, airborne dust, blood, and urine were collected from residents of two neighboring sites in Ubon Ratchathani province, Thailand. Multiple electronic waste-handling activities are conducted in the first site, while the second site is mostly agricultural. Concentrations of chromium, mercury, nickel, and lead in house dust and airborne dust were higher in the electronic waste-handling site (p < 0.05), but levels of exposure were similar in subjects with and without asthma. Although we did not find an association between exposure to these metals and the prevalence of asthma, control measures should be implemented to reduce health risks from long-term exposure to heavy metals.

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“…Recent reports of cadmium in electronic waste (e.g., cell phones and computers) and inexpensive jewelry have increased public awareness regarding this toxic metal (Weidenhamer et al, 2011; Song and Li, 2015; Xu et al, 2015). Electronic waste is one of the fastest growing types of waste globally and due to the ongoing demand for cadmium in electronics, this metal continues to leach into the environment.…”

Section: Introductionmentioning

confidence: 99%

Pleiotropic roles of Ca+2/calmodulin-dependent pathways in regulating cadmium-induced toxicity in human osteoblast-like cell lines

Burwell

Goodwin

et al. 2016

Toxicology Letters

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The heavy metal cadmium is a widespread environmental contaminant that has gained public attention due to the global increase in cadmium-containing electronic waste. Human exposure to cadmium is linked to the pathogenesis of osteoporosis. We previously reported cadmium induces apoptosis and decreases alkaline phosphatase mRNA expression via extracellular signal-regulated protein kinase (ERK) activation in Saos-2 bone-forming osteoblasts. This study examines the mechanisms of cadmium-induced osteotoxicity by investigating roles of Ca+2/calmodulin-dependent protein kinase (CAMK) pathways. Saos-2 or MG-63 cells were treated for 24 or 48 h with 5 μM CdCl2 alone or in combination with calmodulin-dependent phosphodiesterase (PDE) inhibitor CGS-9343β; calmodulin-dependent kinase kinase (CAMKK) inhibitor STO-609; or calmodulin-dependent kinase II (CAMKII) inhibitor KN-93. CGS-9343β protected against cadmium-induced toxicity and attenuated ERK activation; STO-609 enhanced toxicity and exacerbated ERK activation, whereas KN-93 had no detectable effect on cadmium-induced toxicity. Furthermore, CGS-9343β co-treatment attenuated cadmium-induced apoptosis; but CGS-9343β did not recover cadmium-induced decrease in ALP activity. The major findings suggest the calmodulin-dependent PDE pathway facilitates cadmium-induced ERK activation leading to apoptosis, whereas the CAMKK pathway plays a protective role against cadmium-induced osteotoxicity via ERK signaling. This research distinguishes itself by identifying pleiotropic roles for CAMK pathways in mediating cadmium’s toxicity in osteoblasts.

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E-waste environmental contamination and harm to public health in China

Cited by 77 publications

References 51 publications

The Impact of E-waste Occupational Exposure on Male Reproductive Health

The Impact of E-waste Occupational Exposure on Male Reproductive Health

Exposure to Heavy Metals in Electronic Waste Recycling in Thailand

Pleiotropic roles of Ca+2/calmodulin-dependent pathways in regulating cadmium-induced toxicity in human osteoblast-like cell lines

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