Chemicals

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Arsenic

Several reports have described arsenic poisoning of pregnant women after the first trimester. In most cases the newborn babies were healthy, even if the mother developed toxic encephalopathy. However, premature delivery of newborns who died shortly after being born has also been reported (Bollinger 1992, Daya 1989, Lugo 1969, Kantor 1948). Recently, elevated arsenic in drinking water has been associated with a higher risk for anemia in pregnancy and reduced birth weight (Hopenhayn 2006, 2003, Yang 2003). Exposed populations in Chile (40pg/I) and Taiwan (up to 3 mg/1) were compared to non-exposed (<1 ng/1). Such elevated levels of arsenic in drinking water are often associated with pollution from rock formations in the region, e.g. granite. Other sources of arsenic can be from manufacturing processes - for example, the production of copper.

Carbon monoxide

Carbon monoxide (CO) crosses the placenta and can reach concentrations in the fetal blood comparable to those in the mother's. Empirical observations, animal experiments, and theoretical models show that a delay of several hours can be expected in fetuses accumulating and also reducing CO levels. Only after about 14-24 hours is a balance reached. The elimination half-life in a fetus is four to five times longer than in the mother (survey in Barlow 1982).

The risk l'or CNS damage in a fetus is increased if the mother was somnolent or lost consciousness, symptoms corresponding to intoxication stages 4 or 5, even if she recovered soon afterwards. Mental and motor retardation or even severe cerebral damage is possible in such infants. The mature fetus reacts more sensitively to CO intoxication than does the embryo during organogenesis.

A slight acute exposure of the mother with transitory light symptoms like headache and nausea (corresponding to stages 1-2), or chronic exposure to CO (such as is measured in smokers who use one packet of cigarettes per day, or occurs with a concentration of 30ppm in a room or in city air resulting from a working place or environmental sources), is associated with a COHb-concentration of 2-10% in the mother and does not distinctly correlate with fetal damage (Koren 1991, survey in Barlow 1982). The fetus of a smoker, however, does not tolerate additional CO exposure; its capacity to compensate might already be exhausted.

For almost 80 years (see Maresch 1929) there have been reports about CO poisoning in pregnancy that describe inconspicuous courses as well as fetal deaths and CNS defects (Aubard 2000, Kopelman 1998, own observations). A recent study covered 582 women, of whom 54% had not experienced any loss of consciousness. All were treated with hyperbaric oxygen. The maternal outcome was death in two patients and long-term manifestations in four - no different from the outcome in non-pregnant CO-poisoned women. An evaluation of fetal outcome was possible in 515 cases. Fetal death occurred in 15 cases, and 486 pregnancies ended with the delivery of a normal baby. Malformations were observed in 13 babies, which is not a significantly increased rate (Mathieu-Nolf 2006).

In summary, apart from CNS damage, teratogenic effects resulting from CO intoxication are unlikely.

Concerns about oxygen toxicity (retinopathy, premature closure of ductus arteriosus, etc.) resulting from (hyperbaric) oxygen treatment after CO poisoning were discussed, but not confirmed (Mathieu-Nolf 2006, Silverman 1997). In any case, not treating severe CO intoxication would be a far greater risk for the fetus.

Recommendation. Because of the much delayed kinetics of CO in the fetal organism and the higher risk of hypoxic CNS damage to the child resulting from this delay, hyperbaric oxygen treatment of pregnant women with severe CO intoxication must be considered at an early stage. The therapy should be performed for longer than suggested by the symptoms and the CO concentration. Every pregnant woman with reduced consciousness resulting from CO and with a COHb-concentration >20%, or with a deviant fetal heart rate (decelerations, tachycardy, loss of modulation), must be treated with hyperbaric oxygen as quickly as possible and be given 100% oxygen until the start of therapy. As CO reaches the fetus with a considerable delay and phases out only slowly, treatment should be started even after a delay of many hours and after spontaneous improvement of maternal symptoms.

Poisoning with methanol during pregnancy can secondarily damage the fetus, if the acidosis is of long duration. Although methanol crosses the placenta, the fetus seems to be relatively well-protected at first owing to its slower metabolism of methanol into its toxic metabolites like formaldehyde. The classical therapy with intravenous ethanol exposes the fetus to alcohol, and is therefore not totally harmless because of the possible neurological consequences seen with binge drinking and tocolysis with alcohol (Nulman 2004). This is why fomepizol has been suggested more recently as an alternative antidote (Velez 2003). At any rate, neither with methanol nor with ethylene glycol intoxication should (alcohol) therapy be withheld because of a pregnancy (Tencnbein 1997). A report on a case of methanol intoxication during late pregnancy describes a healthy newborn after the treatment of the mother with ethanol, hemodialysis, and alkalinization (Hantson 1997), In another case report, the mother and the child (who was delivered by cesarean section in week 30) died some days after the birth. Alcohol therapy was started in the acidotic mother (pH 7.17) after 36 hours, and only on the third day was she treated with fomepizol. The blood of the acidotic newborn (pH 6.9) had 61.6mg/dl of methanol - a concentration similar to that in the mother (Bclson 2004).

Organophosphorus pesticides

Some reports describe accidental and suicidal overdoses with different outcomes. One mother in her nineteenth week of pregnancy reported that she had no longer felt any movements of the baby 2 hours after having taken chlorpyrifos with suicidal intent. Not earlier than 10 hours after the initial gastric lavage, intensive therapy was started. In the meantime, the fetus had died. Besides a low level of pseudocholinesterase in the mother, the fetal blood contained a high concentration of chlorpyrifos. Some further cases of organophosphorus intoxication of pregnant women ended with the delivery of healthy children. In these cases, therapy with (among others) atropine and pralidoxime was quickly initiated (Kamha

2005, Sebe 2005A). One of these children developed without any problems until at least the age of 4 years.

In reports on nine pregnant women who had taken larger amounts of the herbicidc paraquat, no fetus and only two mothers survived the intoxication. The concentration of paraquat was higher in the fetus' than in the mother's serum {Talbot 1988). Another report describes the intake of 80-100 ml paraquat with suicidal intent in the sixth week of pregnancy. The mother was treated with hemodialysis. The pregnancy seemed to progress without problems; however, it was terminated in the ninth week. Paraquat was found in the fetal tissues (0.25|<g/g) and in the amniotic fluid (0.05)ig/ml). The concentration in the mother's serum was said to be clearly lower at Lhis time (initially 4.8pg/ml was measured). The authors discuss the higher protection of the embryo against paraquat in comparison to the mature fetus. They point out that, especially with intoxication during later pregnancy, the fetus (who is at that stage more endangered anyway) represents an at-risk "reservoir" of paraquat which could return to the mother, and that under these circumstances a therapeutic abortion should be considered (Tsatsakis 1996). One exception is the report about a term birth of a healthy girl, who developed normally until at least the age of 5 years, and whose mother had taken an overdose of paraquat in the twenty-seventh week of pregnancy. She was treated with carbon hemoperfusion, high-dose cyclophosphamide, and methylprednisolone (Jenq 2005).

About 20 cases of thallium ingestion, with suicidal intent or to provoke an abortion, have been reported. A case of chronic intoxication by a rodenticidc containing thallium at the workplace has also recently been described. Most of the children survived the poisoning of their mother, if she was treated adequately. Apart from alopecia, premature delivery and intrauterine growth retardation (but no birth defects) seem to be possible effects of prenatal exposure, including the first trimester (Hoffmann 2000).

Water intoxication

There are some sporadic reports about water intoxication during delivery - for example, the case of a baby aged 6 hours presenting with seizures and hyponatremia (121 mmol/l; mother, 126 mmol/1). The mother had consumed 31 of water shortly before delivery. The further development of the child was uneventful (West 2004).

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