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Skip to main content. Environmental health. Home Environmental health. Hazardous waste. Actions for this page Listen Print. Summary Read the full fact sheet. On this page. Hazardous wastes are wastes or products that have the potential to harm humans or the environment, either now or in the future. There are many options to help you dispose of household hazardous wastes safely, protect the environment and keep your home safe. Recycling programs are available for some hazardous wastes.
Over the last two decades, there have been major changes to the way Australians manage their waste. Recycling has increased but so has the amount of waste we are generating, including the quantity of hazardous waste.
Household hazardous waste The average Australian household stores many hazardous substances or products that contain harmful elements. It can be dangerous to dispose of hazardous wastes through regular rubbish collections.
Examples of household hazardous waste include: Solvent-based paints Pesticides and other garden chemicals Batteries for example car, mobile phone or regular household batteries Motor oils for example from cars or mowers Petrol and kerosene Cleaning and polishing chemicals Swimming pool or spa bath chemicals Pharmaceuticals all medicines Obsolete computer equipment Thermometers, barometers, thermostats, fluorescent tubes and compact fluorescent globes CFLs.
Handling and storage suggestions To handle hazardous waste at home safely you should: Keep the goods in their original containers if possible. If containers are leaking, use new containers but never use food containers like soft drink bottles. Store goods upright with lids secured tightly and out of the reach of young children. Keep all ignition sources, such as matches, well away from the storage area.
Keep the storage area cool and dry. Buy the smallest amount for your needs. How to dispose of hazardous waste Always store hazardous wastes properly while waiting for a suitable disposal method. There are various schemes in Victoria to recycle and dispose of household hazardous waste. For example: Computers — materials used to make computer equipment contain valuable resources that can be re-used. They also contain hazardous materials that could pose a threat to the environment if they are not disposed of in a responsible manner.
In Victoria, unwanted computer equipment — monitors, keyboards, laptops, CD and disc drives — can be recycled through the Byteback scheme. The estimated levels of exposure might be sufficient to generate acute and chronic adverse effects, such as a decrease in Intelligence Quotient IQ [ 6 ]. Chatman-Stephens and colleagues analyzed hazardous waste sites in three Asian countries India, Indonesia, Philippines and estimated approximately 9 million people to be at risk; adding another estimated 43 million people at risk from unscreened sites to the exposed population, 4 million DALYs disability-adjusted life years associated with hazardous waste sites were estimated as the impact [ 7 ].
The remaining waste ends up in illegal dumps [ 11 ]. Africa is also one of the main destinations of illegal transboundary trade of urban and hazardous waste from industrialized countries [ 2 ].
E-waste contains recognized hazardous substances that may be directly released or generated after disposal or during the recycling process. In recent years, investigations reporting a wide spectrum of health risks for local populations living in the areas surrounding hazardous waste dumping sites have been published. Still, an up-to-date evaluation of the evidence of the association between adverse health effects and hazardous waste is not available.
A relationship was suggested with adverse pregnancy outcomes, i. However, the authors considered that the studies were still too few to draw conclusions regarding causality. The evidence, somewhat stronger for reproductive outcomes than for cancer, is not sufficient to establish the causality of the association. The Report deals with landfills at large and not specifically with hazardous waste management; some case-studies, though, address this issue and recommendations about study design are provided [ 14 ].
A review on cancer epidemiology studies of populations resident close to toxic waste sites concluded that available studies provided valid hypotheses, but cannot determine whether residence near toxic waste sites causes an increased cancer risk [ 15 ].
A subsequent review of the literature on health impact of municipal waste management assessed the evidence of association with urban waste landfills as limited for total, neural tube and genitourinary birth defects, and low birth weight [ 16 ].
Consistent conclusions were reached by Mattiello and colleagues [ 17 ]. In this context, a systematic review is presented to evaluate the evidence of health impact of hazardous waste exposure, applying a priori defined criteria. As recently recommended by authoritative agencies, such as the US EPA and WHO [ 18 , 19 , 20 , 21 ], established methods and selection criteria defined a priori were applied.
A five-step process, as described by Woodruff, was followed: 1. Specify the research question; 2. Carry out the literature search, specifying the search strategy with sufficient detail so that it can be reproduced; 3. Select studies for inclusion, analyzing their compliance with a priori defined criteria; 4.
Assess the quality of individual selected studies; 5. Rate the confidence in the body of evidence for each outcome [ 20 ]. In detail:. Boolean operators were used to combine exposure and outcome terms, as reported in the tables. The search was limited to the articles published in the — period, i. Select studies for inclusion.
Original epidemiological studies on populations residentially exposed to hazardous waste were considered; the criteria for inclusion of articles in the review were defined a priori.
Reviews and economic evaluations were not included in the evidence evaluation, but considered subsequently for discussion purposes. Biomonitoring and toxicological studies were not considered as part of the main body of primary evidence, but were retained for interpreting and evaluating the findings of epidemiological investigations.
Each study identified in the initial literature search was assessed for inclusion independently by two investigators. Assess the quality of individual studies.
The full team of investigators established the reliability of each study. This step involved an evaluation of the possible role of chance random error and bias systematic error , arising from flawed exposure and outcome assessment, confounding factors or study design leading to selection bias.
This evaluation was performed individually by one investigator per paper and, subsequently, discussed by the overall group. The reliability of each study was defined in 5 classes, from low 1 to high 5. Rate the strength of the body of evidence, for each outcome.
The evaluation of the evidence of association between each health outcome and hazardous waste exposure was estimated taking into account the reliability of each study, the magnitude and the accuracy of the estimated association, and the concordance between study findings. Alternative explanations, in particular the role of random variability, bias, confounding factors, can be reasonably excluded.
The force of association, considerations on dose-response relationship, time coherence and biological plausibility further support causality. Among the concurring different risk estimates, the results of higher quality studies was given higher weight.
A role of random variability, bias and confounding factors may not be completely excluded. Two thousand five hundred ninety three records were retrieved from MedLine and EMBASE text-word and descriptor searching; of these were excluded because published before Of the remaining records, were excluded on the basis of title and abstract, because not responding to the a priori defined PECO question.
The abstracts of the resulting papers were then evaluated independently by two investigators on the basis of the inclusion criteria. The results of this first evaluation were reviewed by the full team of investigators. Following a review of the full-text of each study, were considered not relevant and were excluded. Most of the selected studies reported more than one health outcome. Altogether, the association between 95 health outcomes diseases and disorders and residential exposure to hazardous waste sites was reported on.
As a result, the evidence of the causal association between hazardous waste related exposures and chronic and reproductive health outcomes was evaluated as: limited, for liver, breast, testis and bladder cancers, non-Hodgkin lymphoma and asthma Additional file 1 : Table S1 , overall and specific congenital anomalies urogenital, neural tube, musculoskeletal and connective system , low birth weight and pre-term birth Additional file 2 : Table S2 ; inadequate, for all the other health outcomes.
Studies on acute effects in populations living near illegal dump sites in Abidjan [ 23 , 24 ] provided sufficient evidence of association between exposure to oil industry waste and general and neurological acute symptoms, and specifically otolaryngological, respiratory, digestive and dermatological symptoms Additional file 3 : Table S3.
The present review considers literature pertaining sites where hazardous waste was handled without control or suitable environmental management. These practices take place both in high and low-middle income countries. However, they occur more frequently in the latter, through illegal dumping of hazardous waste, or when waste dumping took place prior to the enforcement of environmental regulations, or in countries where there is no regulation.
In some cases, hazardous waste can be unknowingly present in landfills. Rigourous methodology for systematic and a priori criteria-based reviews was used. In order to evaluate the strength of study results, and their risk of bias, exposure and outcome assessment methods, confounding control and study design were considered. Ecological studies, however, have played a major role in the investigation of etiological associations of public health importance [ 22 , 25 ]. Data about the contaminants present in the waste site at the time of the study and in the surrounding residential environment was rarely available.
When it was, a higher weight was assigned to the study. Furthermore, the definition of hazardous waste limits comparability between studies. Hazardous waste includes a broad range of contaminants affecting different environmental matrices and involving several routes of exposure, depending on types of waste and hydrogeological and meteorological factors. These limitations tend to underestimate, rather than overestimate, the magnitude of health effects, thus diluting the evidence for specific types of hazardous waste exposure.
The evidence of the association between general and neurological acute symptoms, in particular those regarding otolaryngological, respiratory and digestive systems and the skin, and exposure to oil industry waste releasing high concentrations of hydrogen sulphide was evaluated as sufficient. This evaluation was based on two cross-sectional studies performed in the population resident in Abidjan near the sites where approximately tons of hazardous waste was illegaly dumped and subsequently emitted hydrogen sulphid into the air [ 23 , 24 ].
They consistently reported elevated relative risks, with good accuracy. Furthermore, strength of association, presence of a dose-response relationship, time coherence and biological plausibility support causality. Alternative explanations, in particular the role of random variability, systematic bias and confounding factors, can be reasonably excluded.
Contaminants emitted or released by hazardous waste might play a role for the occurrence of diseases with multi-factor etiology, however evidence of an association was limited, as in the case of liver cancer. In the above-mentioned review of municipal waste management, inadequate evidence was attributed to the association between liver cancer and landfills [ 16 ].
B and C hepatitis viruses, alcohol consumption, tobacco smoking and aflatoxins are the main ascertained risk factors for liver cancer. Exposure to vinyl chloride and 1,2-dichloropropane was defined by IARC as associated with hepatic cancer with sufficient evidence.
The evidence regarding the association of arsenic and its inorganic compounds, DDT, dichloromethane and trichloroethylene was defined as limited [ 26 ]. Hepatotoxic chemical agents can be both naturally occurring and synthetic; the latter comprise metals, aromatic and halogenated hydrocarbons, chlorinated aromatic and nitro compounds that can, to various extents, be present in or released by hazardous waste [ 29 ]; hepatotoxicity can be related to hepatic carcinogenicity.
Other studies [ 32 , 33 ] regarded areas in which biomonitoring detected presence of dioxins in breast milk of women [ 34 ]. In the latter studies the synergistic effects between different risk factors, including B hepatitis virus and hazardous waste contaminants, may be reasonably hypothesized.
We attributed limited evidence to the association between bladder cancer and hazardous waste on the basis of ten articles. The previous review by Porta defined the association between bladder cancer and urban waste disposals as limited [ 16 ]; another review found bladder cancer among those reported in excess in more than one study [ 13 ]. A specific association between bladder cancer and benzo a pyrene was reported elsewhere [ 35 ]. Some of the ten articles on bladder cancer considered in the present review reported the presence of contaminants associated with bladder cancer in the study areas.
Dioxins were detected in biomonitoring studies in Campania waste sites [ 34 ] located in towns where increased bladder cancer risk was reported [ 32 , 33 ]. Several chemical agents were defined as risk factors for NHL with limited evidence: benzene, ethylene oxide, 2,3,7,8-tetrachlorodibenzo-para-dioxin TCDD , PCBs, tetrachloroethylene, trichloroethylene, polychlorophenols and their sodium salts [ 39 ].
For breast and testis cancers, the evidence was evaluated taking into account similarities in their biological characteristics. Limited evidence attributed to breast and testis cancers is based on the etiological plausibility of their relationship with endocrine disruptors EDCs. This evaluation is corroborated by the results found for urogenital tract defects. A role of exposure to EDCs was hypothesized in incidence of breast and testis cancers and urogenital tract anomalies [ 40 ]: positive results for these outcomes in the selected studies and the possible presence of these contaminants in hazardous waste sites support the hypothesis of a causal relationship.
A European case-control study on occupational exposure to endocrine disrupting chemicals in male breast cancer suggested a possible role of occupational exposures to oil and petroleum solvents in motor vehicle mechanics and to chemicals such as alkylphenolic compounds [ 41 ]. IARC defined as limited the association between breast cancer and the exposute to dioxins, ethylene oxide and PCBs [ 26 ]. In our review, five articles on breast cancer were considered, including the above-mentioned studies on areas with documented contamination [ 31 , 32 , 36 ] and an article on populations living in zip code areas near Superfund sites polluted by volatile organic compounds including chloroethenes, chloroethanes, chloromethanes, chlorobenzenes, benzene, toluene, ethyl benzene, xylene [ 42 ].
For testis cancer, IARC assessed limited evidence for DDT, diethylstilbestrol exposure in utero , N,N-dimethylformamide, perfluorooctanoic acid; no agents were defined as associated with testis cancer with sufficient evidence [ 26 ]. An etiological role of exposure to endocrine disruptors in the onset of testis cancer was hypothesized [ 43 ] and suggested in some reviews [ 44 , 45 ].
A possible association between endocrine disruptors and testicular cancer could be explained by the Testicular Dysgenesis Syndrome, reflecting a hormonal imbalance due to environmental or life-style factors during early fetal development [ 40 , 46 , 47 ] and during puberty due to the ingestion of contaminated milk [ 47 ].
Finally, evidence of hazardous waste effects on asthma and adverse reproductive effects was considered limited. Atmospheric particles, including acid aerosols derived from sulfur dioxide emissions, have been linked with worsening of symptoms, reduction in lung function, increased hospital admissions for asthma and increased use of medication.
A Report of the US Department of Health and Human Services defined the evidence of the causal role of active and second-hand smoke, in the incidence and exacerbation of asthma as sufficient or suggestive in different sub-groups of the population [ 52 ].
Therefore, it is plausible that hazardous waste emitting air pollutants might cause asthma in susceptible subjects or exacerbate asthma cases. Diabetes and infectious respiratory diseases, for which the evidence of association with hazardous waste was evaluated as inadequate, deserve some considerations. Two studies included in our review reported consistent findings of an increased risk for diabetes.
Taking into account the high prevalence of the disease and the need to thoroughly assess the role of its many ascertained risk factors, the evaluation of the role of environmental exposures is challenging. A recent systematic review indicated a positive association between diabetes and serum concentrations of several pollutants such as polychlorinated dibenzodioxins and dibenzofurans, PCBs, and several organochlorine pesticides [ 54 ].
Type 2 diabetes has recently been recognized as a risk modifier for PM health effects, enhancing mortality risks associated with PM exposure [ 51 ]. The evidence of a causal association between the risk of diabetes and active smoking was defined as sufficient, with a positive dose-response relationship with the number of cigarettes smoked [ 52 ].
However, consistent results of increased risk were reported near waste sites with air emissions of POPs [ 48 , 49 ]. Taking into account the available evidence on health effects of air pollution [ 51 ], these results require further confirmation, notably in populations living near hazardous waste that emits air pollutants.
Regarding congenital anomalies CAs , the evidence of association to hazardous waste was evaluated as limited for overall and some subgroups of CAs i. These findings are consistent with previous reviews [ 13 , 16 , 17 ]. Our update confirms some limitations mainly due to the small number of studies and weak exposure assessment. As CAs are short-term latency outcomes, they are important for investigating short-term effects in polluted areas.
The etiology of CA is multi-factorial, with an important role of genetic factors, and a recognized interaction between genetic and environmental factors [ 55 ] and epigenetic mechanisms; this topic deserves further investigation in order to better clarify the etiological pattern. Despite this, the reported risk estimates are often not accurate. Furthermore, the interpretation of results regarding groups of CAs with different causes is difficult and requires caution [ 56 ].
Two of the reviewed studies investigated the association between exposure to hazardous waste and hypospadias. This association is of interest since the vast majority of cases seem to have multi-factorial aetiology, with many genetic and environmental factors playing a role, in particular endocrine-disrupting chemicals [ 57 , 58 , 59 ]. Our results are in agreement with a recent review claiming that the literature is currently poor and does not support a conclusive judgment on environmental contaminants and congenital anomalies in the general population [ 60 ].
Among the five studies considered for pre-term birth evaluation only two were evaluated as high quality, and although the estimated risks were above unity for all the studies, none reached statistical significance, except in the study of Love Canal residents, who had a significant risk of pre-term birth compared to New York State reference rates.
The studies on low birth weight LBW were more numerous; among the nine studies considered, one was of high quality, reporting no significantly increased risks [ 61 ], and two were of moderate-high quality and reported statistically significant excess of risk [ 62 , 63 ]. Although the body of evidence is richer than for pre-term birth, we believe that it is still not enough to upgrade the evaluation of limited evidence previously assigned by Porta [ 16 ] and Mattiello [ 17 ] for the association with landfills of urban waste.
The present review highlighted that there is sufficient evidence of association between exposure to oil industry waste releasing high concentrations of hydrogen sulphide and acute symptoms. The evidence of causal relationship with hazardous waste was defined as limited for: liver, bladder, breast and testis cancers and non-Hodgkin lymphoma.
Among non-neoplastic diseases, asthma was found to be related to hazardous waste with limited evidence. We evaluated as limited the evidence of the association between the exposure to hazardous waste and adverse birth outcomes, including low birth weight, pre-term birth, congenital anomalies overall and anomalies of the urogenital, connective and musculoskeletal systems.
The evidence of a causal relationship was defined as inadequate for most other health outcomes. The available evidence of the health effects of specific contaminants present in some hazardous waste corroborates our evaluation. In particular, drawing from the evidence described in the previous section: persistent organic pollutants, in particular benzene and those chlorinated, i.
These data confirm that hazardous waste, if not suitably managed, might cause adverse health effects on populations living near the sites where they are dumped or processed. The contamination of different environmental matrices, including food, water, soil and air, represents a health risk for these populations. A strong contrast to illegal trade and the deployment of sound management practices is warranted as a priority — no further evidence is needed.
In several instances, however, further investigation is warranted to fill important knowledge gaps: in particular, population studies analysing different pathways of exposure, taking into account the characteristics of the site and the contaminants present in each waste site, might provide useful information. Acute respiratory diseases, diabetes and childhood neurological disorders are of particular interest, also in consideration of the strong indications that environmental exposures to EDCs and potential EDCs can cause cognitive and behavioural deficits in humans [ 40 ].
The results of our review, although not conclusive, provide indications that public health policies on hazardous waste management are urgently needed. International, national and local authorities should oppose and eliminate poor, outdated and illegal practices of waste disposal including illegal transboundary trade , which still affect some communities in industrialized and middle-low income countries, and implement and enforce regulation.
Compliance with the Basel Convention on the Control of Transboundary Movements of Hazardous Wastes and their Disposal is necessary to prevent high exposures and consequent health effects, particularly among the vulnerable and the poor [ 64 ].
World Health Organization. Waste and human health: evidence and needs. Bonn, Germany. Google Scholar. Health risks from hazardous waste disposal: the need for international scientific cooperation. Eur J Oncol. Environ Health Perspect. When chemicals make their way into our rivers and lakes, they make this water unsafe for drinking. The water is also unsafe to use for agricultural purposes.
Animals drinking this water will get sick and die, and plants that rely on the water will be destroyed. Ultimately, the hazardous waste will have limited the ability of the surrounding ecosystem to survive.
Some hazardous waste is flammable. It has the potential to ignite or explode, causing a fire. In the wrong circumstances, this could result in widespread wildlife death and damage to the environment, which could take years to put right. More long-term effects on the environment include signs of mutation in animals. Evidence has been released suggesting certain fish that habitually swim in severely polluted estuaries along the US East Coast, have mutated to develop a strong resistance to hazardous waste.
However, other substances begin to have a significant impact after a certain period and prolonged exposure. As an example, we can look to toxins such as lead and mercury. When these toxins are present in the environment for many years, they accumulate.
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