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| {{Header}} | | {{Header}} |
| ==Introduction== | | ==Introduction== |
| | [[File:Particulate matter.jpg|thumb|300px|Particulate matter comparative size]] |
| [[File:Metal_contamination.jpg|thumb|300px]] | | [[File:Metal_contamination.jpg|thumb|300px]] |
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| ''Draft Page - Notice removed when completed.''
| | Air pollution has recently been identified through statistical studies to be involved with abnormal development (See also {{smoking}}). With industrialisation and vehicle produced air pollution, it can consist of particulate matter, {{heavy metals}} and a range of {{Chemicals}}. |
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| Air pollution has recently been identified through statistical studies to be involved with abnormal development (See also {{smoking}}). With industrialisation and vehicle produced air pollution, it can consist of particulate matter, {{heavy metals}} and a range of {{chemicals}}.
| | Vehicle traffic air pollution can consist of several different components including: (elemental carbon, nitrogen dioxide, and ultrafine particle matter (10-700 nm). |
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| ==Some Recent Findings== | | ==Some Recent Findings== |
| | [[File:Yinchuan - China.jpg|thumb|alt=Yinchuan, China|Yinchuan, Ningxia, China]] |
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| | * '''Epigenetic marks of prenatal air pollution exposure found in multiple tissues relevant for child health'''{{#pmid:30826615|PMID30826615}} "Prenatal air pollution exposure has been linked to many adverse health conditions in the offspring. However, little is known about the mechanisms underlying these associations. Epigenetics may be one plausible biologic link. Here, we sought to identify site-specific and global DNA methylation (DNAm) changes, in developmentally relevant tissues, associated with prenatal exposure to nitrogen dioxide (NO2) and ozone (O3). Additionally, we assessed whether sex-specific changes in methylation exist and whether DNAm changes are consistently observed across tissues. RESULTS: We identified global and locus-specific changes in DNA methylation related to prenatal exposure to NO2 and O3 in 2 developmentally relevant tissues. Neonates with increased prenatal O3 exposure had lower aggregate levels of DNAm at CpGs located in open sea and shelf regions of the genome. We identified 6 DMRs associated with prenatal NO2 exposure, including 3 sex-specific. An additional 3 sex-specific DMRs were associated with prenatal O3 exposure levels. DMRs initially detected in cord blood samples (n = 4) showed consistent exposure-related changes in DNAm in placenta. However, the DMRs initially detected in placenta (n = 5) did not show DNAm differences in cord blood and, thus, they appear to be tissue-specific. CONCLUSIONS: We observed global, locus, and sex-specific methylation changes associated with prenatal NO2 and O3 exposures. Our findings support DNAm is a biologic target of prenatal air pollutant exposures and highlight epigenetic involvement in sex-specific differential susceptibility to environmental exposure effects in 2 developmentally relevant tissues." {{Epigenetics}} |
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| | * '''The association between maternal exposure to ambient particulate matter of 2.5 μm or less during pregnancy and fetal congenital anomalies in Yinchuan, China: A population-based cohort study'''{{#pmid:30455103|PMID30455103}} "Few studies from western countries have linked prenatal exposure to ambient particulate matter <2.5 μm (PM2.5) with increased risk of congenital anomalies. However, the results are mixed. Particularly, evidence is limited for Chinese pregnant women. METHODS: In this retrospective cohort study, we matched the data of all pregnant women laboured in public hospitals during 2015-2016 in Yinchuan, a capital city of northwest China and the data of daily average PM2.5, nitrogen dioxide (NO2), sulphur dioxide (SO2) and ozone (O3) concentrations of the nearest monitor station. We calculated a time-dependent exposure over the entire pregnancy for each woman. We used a time varying Cox proportional hazards model to explore the association between PM2.5 exposure and the risk of congenital anomalies, after adjusting for individual confounders and other pollutants. RESULTS: A total of 39,386 singleton live births were included in the study, and 530 (1.35%) were with congenital anomalies. An increase of 10 μg/m3 in PM2.5 exposure over the entire pregnancy was significantly associated with increased risk of congenital anomalies, with hazard ratio (HR) of 1.35 [95% confidence interval (95%CI): 1.16, 1.58]. For subtype analyses, PM2.5 exposure exhibited a significant association with cardiac anomalies and other unclassifiable anomalies, with HRs of 1.60 (95%CI: 1.24, 2.08) and 1.42 (95%CI: 1.07, 1.89), respectively. The impacts of PM2.5 exposure on orofacial anomalies and musculoskeletal anomalies were not significant. CONCLUSION: Our results indicate high concentration of PM2.5 could increase the risk of congenital anomalies among Chinese, especially for cardiac anomalies. Self-protective measures involving reducing PM2.5 pollution exposure during pregnancy as well as environmental policies aiming to restrict PM2.5 emission could be helpful to reduce the burden of cognitional anomalies." |
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| | * '''Air Pollution Exposure During Fetal Life, Brain Morphology, and Cognitive Function in School-Age Children'''{{#pmid:29530279|PMID29530279}} "Air pollution exposure during fetal life has been related to impaired child neurodevelopment, but it is unclear if brain structural alterations underlie this association. The authors assessed whether air pollution exposure during fetal life alters brain morphology and whether these alterations mediate the association between air pollution exposure during fetal life and cognitive function in school-age children. We used data from a population-based birth cohort set up in Rotterdam, The Netherlands (2002-2006). Residential levels of air pollution during the entire fetal period were calculated using land-use regression models. Structural neuroimaging and cognitive function were performed at 6 to 10 years of age (n = 783). Mean fine particle levels were 20.2 μg/m3 (range, 16.8-28.1 μg/m3). CONCLUSIONS: Exposure to fine particles during fetal life was related to child brain structural alterations of the cerebral cortex, and these alterations partially mediated the association between exposure to fine particles during fetal life and impaired child inhibitory control. Such cognitive impairment at early ages could have significant long-term consequences." |
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| | * '''Association between traffic-related air pollution in schools and cognitive development in primary school children: a prospective cohort study'''{{#pmid:25734425|PMID25734425}} "Air pollution is a suspected developmental neurotoxicant. Many schools are located in close proximity to busy roads, and traffic air pollution peaks when children are at school. We aimed to assess whether exposure of children in primary school to traffic-related air pollutants is associated with impaired cognitive development. METHODS AND FINDINGS: We conducted a prospective study of children (n = 2,715, aged 7 to 10 y) from 39 schools in Barcelona (Catalonia, Spain) exposed to high and low traffic-related air pollution, paired by school socioeconomic index; children were tested four times (i.e., to assess the 12-mo developmental trajectories) via computerized tests (n = 10,112). CONCLUSIONS: Children attending schools with higher traffic-related air pollution had a smaller improvement in cognitive development." |
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| ==Metal Toxicity==
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| | Heavy Metals Toxicity (Table: U.S. GEOLOGICAL SURVEY CIRCULAR 1133, 1995)
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| In another recent study using the sea urchin embryo, Japanese researchers have identified a hierarchy of toxic effects from different heavy metals.
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| "Interactive toxic effects between heavy metals were investigated using a sea urchin (Anthocidaris crassispina) bioassay. An effluent from an abandoned mine showed significant inhibitory effects on embryo development as well as producing specific malformations. The effects on the embryos were reproduced by synthetic polluted seawater consisting of eight metals (manganese, lead, cadmium, nickel, zinc, chromium, iron, and copper) at the concentrations detected in the mine effluent. This indicated that the heavy metals were responsible for the effects observed. Five heavy metals were ranked in decreasing order of toxicity as follows: Cu > Zn > Pb > Fe > Mn. Among these, zinc and manganese could cause malformation of the embryos. From bioassay results using 27 combinations of heavy metals, 16 combinations including zinc could produce specific malformations, such as radialized, exo-gastrulal, and spaceship Apollo-like gastrulal embryos. Zinc was one of the elements responsible for causing malformations and its effects were intensified by the presence of the other metals, such as manganese, lead, iron, and copper." Naomasa Kobayashia and Hideo Okamurab.
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| ==Metal in Water==
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| A major dilemma is the biological difficulty of clearing heavy metals and the subsequent accumulation of these metals in the food chain mainly from the hydrologic environment.
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| [[File:Heavy_metals_water.gif]]
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| ==Lead==
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| [[File:Lead pipe.jpg|thumb|Lead pipe]]
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| [[File:CDC_Screening_young_children_for_lead_poisoning_cover.jpg|thumb|CDC - Screening young children for lead poisoning]]
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| Lead in the environment is postnatally toxic and prenatally teratogenic.{{#pmid:18075625|PMID18075625}} Lead exposure can occur in industrial and mining and can also be derived from leaded petrol, old lead piping, historic paints, and other environmental sources).
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| For children aged less than 6 years of age the CDC (USA) has defined an elevated blood lead level (BLL) as >10 µg/dL, but also indicated that evidence exists for subtle effects at lower levels. (Links: CDC - Lead Poisoning Prevention Program | Blood Lead Levels in Young Children - United States and Selected States 1996-1999)
| | ==Particulate Matter== |
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| * Lead crosses the placental barrier readily.
| | Fine ambient particulate matter consists of small particles of 2.5 μm or less in size. While ultrafine particle matter occurs in the range of 10-700 nm. |
| * Fetal blood levels are directly proportional to maternal levels.
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| * Lead poisoning affects virtually every system in the body, and often occurs with no distinctive symptoms.
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| * Lead in our diet is mainly found in osseous (bone) structures.
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| * Lead can damage a child's central nervous system, kidneys, and reproductive system and, at higher levels, can cause coma, convulsions, and death.
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| * Even low levels of lead are harmful and are associated with decreased intelligence, impaired neurobehavioral development, decreased stature and growth, and impaired hearing acuity.
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| * CDC has established a national surveillance system for children with elevated blood lead levels.
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| * CDC helped to initiate federal activities to reduce lead in gasoline, which brought about declines in average blood lead levels in the U.S. population. Data from the most recent National Health and Nutrition Examination Survey (NHANES) show that the percentage of U.S. children with elevated blood lead levels has dropped from 88.2% in the late 1970s to 4.4% in the early 1990s. (NHANES Chart)
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| '''Related References'''
| | ==Asthma== |
| * Interrelations of lead levels in bone, venous blood, and umbilical cord blood with exogenous lead exposure through maternal plasma lead in peripartum women{{#pmid:11401766|PMID11401766}}
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| * Effect of breast milk lead on infant blood lead levels at 1 month of age{{#pmid:15471729|PMID15471729}}
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| | Flow limitation during tidal expiration in early life significantly associated with the development of physician-diagnosed asthma by the age of 2 years. Infants with abnormal lung function soon after birth may have a genetic predisposition to asthma or other airway abnormalities that predict the risk of subsequent lower respiratory tract illness. Asthma phenotypes have a number of different classifications; allergic asthma, intrinsic or nonallergic asthma, infectious asthma, and aspirin-exacerbated asthma, and environmental exposures (occupational agents, {{smoking}}, {{air pollution}}, cold dry air).{{#pmid:25439356|PMID5439356}} |
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| :'''Links:''' [[Normal Development - Milk]] | [http://www.cdc.gov/nceh/lead/publications CDC - Childhood Lead Poisoning Publications] | [http://www.unep.org/hazardoussubstances/Home/tabid/197/hazardoussubstances/LeadCadmium/PrioritiesforAction/GAELP/tabid/6176/Default.aspx Global Alliance to Eliminate Lead Paint]
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| ==Mercury==
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| [[File:Mercury.jpg|thumb|Mercury]]
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| Used traditionally in the felting of hats, hence "mad hatters", a more recent example of mercury's toxicity was shown in Japan.
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| Japan had industrial mercury poisoning of waterways by methyl mercury causing Minamata disease, which had substantial neurological effects similar to Hunter Russell syndrome. For more information on mercury the chemical, see Mercury MSDS. There has also been a movie available "Medical Study of Minamata Disease".
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| Australia - Food Standards Australia New Zealand (FSANZ)
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| "FSANZ’s Chief Scientist, Dr Marion Healy, said ‘Our investigations show that the level of mercury in most fish caught and sold in Australia is low."
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| "The Australian Dietary Guidelines advise eating one or two fish meals per week for good health. The good news is that FSANZ has found it is safe for all population groups to eat 2-3 serves per week of most types of fish. There are only a few types of fish, which FSANZ recommends limiting in the diet – these are billfish (swordfish / broadbill and marlin ), shark/flake, orange roughy and catfish." FSANZ updates advice on mercury in fish (Australia only) 18 March 2004 see also [http://www.foodstandards.gov.au/consumerinformation/adviceforpregnantwomen/mercuryinfish.cfm 2 June 2011].
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| :'''Links:''' [http://www.unep.org/hazardoussubstances/MinamataConvention/DiplomaticConference/tabid/105832/Default.aspx Diplomatic Conference for the Minamata Convention on Mercury 2013] | [http://www.env.go.jp/en/chemi/mercury/mcm.html Minamata Convention on Mercury][http://www.foodstandards.gov.au/consumerinformation/adviceforpregnantwomen/mercuryinfish.cfm Australia - food standards] | [http://www.foodauthority.nsw.gov.au/consumers/life-events-and-food/pregnancy/mercury-in-fish-campaign NSW Food Authority] | [http://www.federalregister.gov/articles/2011/05/06/2011-11025/elemental-mercury-used-in-barometers-manometers-hygrometerspsychrometers-significant-new-use-rule#p-3 USA - federal register proposal 2011]
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| ==Chromium==
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| [[File:Chromium.jpg|thumb|Chromium]]
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| Hexavalent chromium (CrVI) is used in more than 50 industries and is an important heavy metal pollutant. A recent study (2005) in monkeys (Macaca radiata) has demonstrated an effect on testicular spermatogenesis, possibly by inducing free radical toxicity. If these effects also occur in humans, then spermatazoa development could also be affected, the study further suggested a supplementation of antioxidant vitamins may be beneficial to the affected subjects.{{#pmid:15980013|PMID15980013}}
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| :'''Links:''' [[Talk:Abnormal_Development_-_Heavy_Metals#chromium|Related References]]
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| ==Cadmium==
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| Cadmium (Cd) is a heavy metal pollutant produced during the smelting of other metals. It has many industrial and domestic uses (some paints, plastics, fertilisers, metal plating) and is founds use in the environment cadmium is in nickel-cadmium (NiCad) rechargeable batteries used in many portable devices as well as being present in cigarette smoke.
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| An animal study has shown that cadmium can induce retinoic acid signaling by regulating retinoic acid metabolic gene expression,{{#pmid:19556237|PMID19556237}} suggesting that cadmium-induced teratogenicity may be due to altering levels of retinoic acid by disrupting the expression of retinoic acid-metabolizing genes. [[Developmental Signals - Retinoid acid]]
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| A recent human study of coastal populations of South Africa{{#pmid:26544567|PMID26544567}} has identified associations between prenatal Cd exposure and birth anthropometry in female neonates but not in male neonates, suggesting a potential sex difference in the toxico-kinetics and toxico-dynamics of Cd.
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| :'''Links:''' [[Developmental Signals - Retinoid acid|Retinoic acid]]
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| ==Lithium==
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| [[File:Lithium.jpg|thumb|Lithium]]
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| Lithium (Li, atomic number 3) is a soft alkali metal found in the natural environment, in industrial products (lithium batteries, some glass and ceramic products) and also is used to treat people with bipolar disorder. Lithium used as a drug, in a salt form, acts on the central nervous system as an antimanic agent to treat episodes of mania (frenzied, abnormally excited mood) associated with bipolar disorders. Lithium has been associated with fetal cardiac teratogenicity possibly by affecting Wnt/beta-catenin signaling.{{#pmid:18418887|PMID18418887}}
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| :'''Links:''' [[Abnormal Development - Drugs]] | [http://www.nlm.nih.gov/medlineplus/druginfo/meds/a681039.html MedlinePlus - Lithium] | [http://www.nlm.nih.gov/medlineplus/ency/article/002667.htm MedlinePlus - Lithium Toxicity] | [http://www.otispregnancy.org/files/lithium.pdf OTIS - Lithium and Pregnancy PDF]
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| ==Yttrium-90==
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| [[File:Yttrium.jpg|thumb|Yttrium]]
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| A therapeutic radioactive form of yttrium used in microspheres for the internal treatment of various liver cancers. As such it would be unlikely to be found in a human development situation.
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| ==Indium==
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| [[File:Indium.jpg|thumb|Indium]]
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| A rare, malleable and easily fusible post-transition metal that is chemically similar to gallium and thallium, and also shows properties intermediate between these two elements. Currently used industrially in liquid crystal displays and touchscreens, and historically in thin-films to form lubricated layers. Medically used in a radioactive form (indium-111) in nuclear medicine tests and as a radio-tracker. Indium is not known to be used by any biological organism. There are some animal teratogenic studies that have looked at the effect of indium salts (indium chloride).
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| :'''Embryotoxic and teratogenic effects of indium chloride in rats and rabbits'''{{#pmid:10681097|PMID10681097}} "Indium was found to cross the placenta and appeared in fetal blood in proportion to the metal concentration of the maternal blood. In the amniotic fluid, indium concentrations remained below the detection limit. ...In rats, the effects of indium chloride causing fetal retardation was found to be independent of exposure time. The teratogenic effects were the highest on d 11 and 12 of gestation, when indium chloride caused gross external malformations. Data suggest that the teratogenic effects of indium chloride can be attributed primarily to a direct cytotoxic action of indium resulting from placental transfer, but the effect is not a selective one, as it appears only in the presence of maternal toxic effects."
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| | A recent Dutch PIAMA birth cohort study has shown that air pollution exposure is associated with a lower lung function in schoolchildren.{{#pmid:30016982|PMID30016982}} |
| ==References== | | ==References== |
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| ===Articles=== | | ===Articles=== |
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| {{#pmid:20024603}}
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| {{#pmid:16648469}}
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| {{#pmid:16124873}}
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| ===Search Pubmed=== | | ===Search Pubmed=== |
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| June 2010 "Heavy Metal Teratogen" All (744) Review (72) Free Full Text (86)
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| '''Search Pubmed:''' [http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=Heavy%20Metal%20Teratogen Heavy Metal Teratogen]
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| == External Links == | | == External Links == |
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| {{Footer}} | | {{Footer}} |
| [[Category:Abnormal Development]] [[Category:Environmental Abnormalities]] [[Category:Hearing Loss]] [[Category:Prenatal Diagnosis]] | | [[Category:Abnormal Development]] [[Category:Environmental Abnormalities]][[Category:Prenatal Diagnosis]] |
Introduction
Particulate matter comparative size
Air pollution has recently been identified through statistical studies to be involved with abnormal development (See also smoking). With industrialisation and vehicle produced air pollution, it can consist of particulate matter, heavy metals and a range of chemicals.
Vehicle traffic air pollution can consist of several different components including: (elemental carbon, nitrogen dioxide, and ultrafine particle matter (10-700 nm).
In addition to their direct toxic effects, the potential reduction in fetal growth and long-term effects should also be considered. Much of the basic research relies on studies in various animal models of development and we should also consider the ongoing development of new industrial products in the environment with unknown or untested effects upon development.
Some Recent Findings
- Epigenetic marks of prenatal air pollution exposure found in multiple tissues relevant for child health[1] "Prenatal air pollution exposure has been linked to many adverse health conditions in the offspring. However, little is known about the mechanisms underlying these associations. Epigenetics may be one plausible biologic link. Here, we sought to identify site-specific and global DNA methylation (DNAm) changes, in developmentally relevant tissues, associated with prenatal exposure to nitrogen dioxide (NO2) and ozone (O3). Additionally, we assessed whether sex-specific changes in methylation exist and whether DNAm changes are consistently observed across tissues. RESULTS: We identified global and locus-specific changes in DNA methylation related to prenatal exposure to NO2 and O3 in 2 developmentally relevant tissues. Neonates with increased prenatal O3 exposure had lower aggregate levels of DNAm at CpGs located in open sea and shelf regions of the genome. We identified 6 DMRs associated with prenatal NO2 exposure, including 3 sex-specific. An additional 3 sex-specific DMRs were associated with prenatal O3 exposure levels. DMRs initially detected in cord blood samples (n = 4) showed consistent exposure-related changes in DNAm in placenta. However, the DMRs initially detected in placenta (n = 5) did not show DNAm differences in cord blood and, thus, they appear to be tissue-specific. CONCLUSIONS: We observed global, locus, and sex-specific methylation changes associated with prenatal NO2 and O3 exposures. Our findings support DNAm is a biologic target of prenatal air pollutant exposures and highlight epigenetic involvement in sex-specific differential susceptibility to environmental exposure effects in 2 developmentally relevant tissues." epigenetics
- The association between maternal exposure to ambient particulate matter of 2.5 μm or less during pregnancy and fetal congenital anomalies in Yinchuan, China: A population-based cohort study[2] "Few studies from western countries have linked prenatal exposure to ambient particulate matter <2.5 μm (PM2.5) with increased risk of congenital anomalies. However, the results are mixed. Particularly, evidence is limited for Chinese pregnant women. METHODS: In this retrospective cohort study, we matched the data of all pregnant women laboured in public hospitals during 2015-2016 in Yinchuan, a capital city of northwest China and the data of daily average PM2.5, nitrogen dioxide (NO2), sulphur dioxide (SO2) and ozone (O3) concentrations of the nearest monitor station. We calculated a time-dependent exposure over the entire pregnancy for each woman. We used a time varying Cox proportional hazards model to explore the association between PM2.5 exposure and the risk of congenital anomalies, after adjusting for individual confounders and other pollutants. RESULTS: A total of 39,386 singleton live births were included in the study, and 530 (1.35%) were with congenital anomalies. An increase of 10 μg/m3 in PM2.5 exposure over the entire pregnancy was significantly associated with increased risk of congenital anomalies, with hazard ratio (HR) of 1.35 [95% confidence interval (95%CI): 1.16, 1.58]. For subtype analyses, PM2.5 exposure exhibited a significant association with cardiac anomalies and other unclassifiable anomalies, with HRs of 1.60 (95%CI: 1.24, 2.08) and 1.42 (95%CI: 1.07, 1.89), respectively. The impacts of PM2.5 exposure on orofacial anomalies and musculoskeletal anomalies were not significant. CONCLUSION: Our results indicate high concentration of PM2.5 could increase the risk of congenital anomalies among Chinese, especially for cardiac anomalies. Self-protective measures involving reducing PM2.5 pollution exposure during pregnancy as well as environmental policies aiming to restrict PM2.5 emission could be helpful to reduce the burden of cognitional anomalies."
- Air Pollution Exposure During Fetal Life, Brain Morphology, and Cognitive Function in School-Age Children[3] "Air pollution exposure during fetal life has been related to impaired child neurodevelopment, but it is unclear if brain structural alterations underlie this association. The authors assessed whether air pollution exposure during fetal life alters brain morphology and whether these alterations mediate the association between air pollution exposure during fetal life and cognitive function in school-age children. We used data from a population-based birth cohort set up in Rotterdam, The Netherlands (2002-2006). Residential levels of air pollution during the entire fetal period were calculated using land-use regression models. Structural neuroimaging and cognitive function were performed at 6 to 10 years of age (n = 783). Mean fine particle levels were 20.2 μg/m3 (range, 16.8-28.1 μg/m3). CONCLUSIONS: Exposure to fine particles during fetal life was related to child brain structural alterations of the cerebral cortex, and these alterations partially mediated the association between exposure to fine particles during fetal life and impaired child inhibitory control. Such cognitive impairment at early ages could have significant long-term consequences."
- Association between traffic-related air pollution in schools and cognitive development in primary school children: a prospective cohort study[4] "Air pollution is a suspected developmental neurotoxicant. Many schools are located in close proximity to busy roads, and traffic air pollution peaks when children are at school. We aimed to assess whether exposure of children in primary school to traffic-related air pollutants is associated with impaired cognitive development. METHODS AND FINDINGS: We conducted a prospective study of children (n = 2,715, aged 7 to 10 y) from 39 schools in Barcelona (Catalonia, Spain) exposed to high and low traffic-related air pollution, paired by school socioeconomic index; children were tested four times (i.e., to assess the 12-mo developmental trajectories) via computerized tests (n = 10,112). CONCLUSIONS: Children attending schools with higher traffic-related air pollution had a smaller improvement in cognitive development."
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| More recent papers
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This table allows an automated computer search of the external PubMed database using the listed "Search term" text link.
- This search now requires a manual link as the original PubMed extension has been disabled.
- The displayed list of references do not reflect any editorial selection of material based on content or relevance.
- References also appear on this list based upon the date of the actual page viewing.
References listed on the rest of the content page and the associated discussion page (listed under the publication year sub-headings) do include some editorial selection based upon both relevance and availability.
More? References | Discussion Page | Journal Searches | 2019 References | 2020 References
Search term: Air Pollution Teratology
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| Older Papers
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| These papers originally appeared in the Some Recent Findings table, but as that list grew in length have now been shuffled down to this collapsible table.
See also the Discussion Page for other references listed by year and References on this current page.
|
Particulate Matter
Fine ambient particulate matter consists of small particles of 2.5 μm or less in size. While ultrafine particle matter occurs in the range of 10-700 nm.
Asthma
Flow limitation during tidal expiration in early life significantly associated with the development of physician-diagnosed asthma by the age of 2 years. Infants with abnormal lung function soon after birth may have a genetic predisposition to asthma or other airway abnormalities that predict the risk of subsequent lower respiratory tract illness. Asthma phenotypes have a number of different classifications; allergic asthma, intrinsic or nonallergic asthma, infectious asthma, and aspirin-exacerbated asthma, and environmental exposures (occupational agents, smoking, air pollution, cold dry air).[5]
A recent Dutch PIAMA birth cohort study has shown that air pollution exposure is associated with a lower lung function in schoolchildren.[6]
References
- ↑ Ladd-Acosta C, Feinberg JI, Brown SC, Lurmann FW, Croen LA, Hertz-Picciotto I, Newschaffer CJ, Feinberg AP, Fallin MD & Volk HE. (2019). Epigenetic marks of prenatal air pollution exposure found in multiple tissues relevant for child health. Environ Int , 126, 363-376. PMID: 30826615 DOI.
- ↑ Liu C, Li Q, Yan L, Wang H, Yu J, Tang J, Yao H, Li S, Zhang Y & Guo Y. (2019). The association between maternal exposure to ambient particulate matter of 2.5 μm or less during pregnancy and fetal congenital anomalies in Yinchuan, China: A population-based cohort study. Environ Int , 122, 316-321. PMID: 30455103 DOI.
- ↑ Guxens M, Lubczyńska MJ, Muetzel RL, Dalmau-Bueno A, Jaddoe VWV, Hoek G, van der Lugt A, Verhulst FC, White T, Brunekreef B, Tiemeier H & El Marroun H. (2018). Air Pollution Exposure During Fetal Life, Brain Morphology, and Cognitive Function in School-Age Children. Biol. Psychiatry , 84, 295-303. PMID: 29530279 DOI.
- ↑ Sunyer J, Esnaola M, Alvarez-Pedrerol M, Forns J, Rivas I, López-Vicente M, Suades-González E, Foraster M, Garcia-Esteban R, Basagaña X, Viana M, Cirach M, Moreno T, Alastuey A, Sebastian-Galles N, Nieuwenhuijsen M & Querol X. (2015). Association between traffic-related air pollution in schools and cognitive development in primary school children: a prospective cohort study. PLoS Med. , 12, e1001792. PMID: 25734425 DOI.
- ↑ Hekking PP & Bel EH. (2014). Developing and emerging clinical asthma phenotypes. J Allergy Clin Immunol Pract , 2, 671-80; quiz 681. PMID: 25439356 DOI.
- ↑ Finke I, de Jongste JC, Smit HA, Wijga AH, Koppelman GH, Vonk J, Brunekreef B & Gehring U. (2018). Air pollution and airway resistance at age 8 years - the PIAMA birth cohort study. Environ Health , 17, 61. PMID: 30016982 DOI.
Reviews
Articles
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Cite this page: Hill, M.A. (2024, April 19) Embryology Abnormal Development - Air Pollution. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Abnormal_Development_-_Air_Pollution
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- © Dr Mark Hill 2024, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G
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