What are the effects on humans of exposure to various toxic gases that are found in buildings?
This document gives basic information about exposure to and potential health hazards from a number of common toxic gases that may be found indoors or in or around buildings. We describe symptoms of exposure to these gases, industry recommendations for gas exposure limits, how gases may be measured, and how to track down and cure the sources of gas leaks in buildings.
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Portions of this material are quoted from comments by Jack Peterson at a public CompuServe safety forum in 1987 when we first visited this topic. The material has been frequently updated through 2016.
Gas exposure hazard evaluation consists of comparing measurements of exposure (or dose) with exposures (doses) known to be safe or known to be hazardous. For the most part, because of biological variation, "no effect" levels are much easier to estimate than are "first effect" or other levels indicative of injury.
Watch out: When considering the possible toxicity or health hazards of exposure to gases in buildings, readers should note that
Of the several industrial hygiene standards-setting groups in this country, the most important and/or most quoted are the National Institute for Occupational Safety and Health (NIOSH), the Occupational Safety and Health Administration (OSHA), and the American Conference of Governmental Industrial Hygienists (ACGIH).
Only those standards promulgated by OSHA (called Permissible Exposure Limits or PELs) have the force of law; the others are advisory except that OSHA has claimed the power to force compliance with NIOSH "Recommended Standards" if it chooses to do so. The main advantage of ACGIH Threshold Limit Values (TLVs) is that they are reviewed and updated annually; neither NIOSH nor OSHA updates its standards with any regular frequency.
Health Hazards of some Gases, Jack E. Peterson, P.E., CIH, Ph.D., May, 1987
Ammonia is very soluble in water and, in water, hydrolyzes to ammonium hydroxide, a strong base. These properties insure that ammonia gas is an upper respiratory tract and eye irritant. It dissolves in the water of mucous membranes (or tears), hydrolyzes and irritates rapidly mainly because of the high pH that results.
Because of this biological property of prompt irritation, most people cannot tolerate a concentration of ammonia in air sufficiently high to be harmful. Its warning properties assure a negligible hazard from ammonia inhalation if escape is possible. As with formaldehyde and other good upper respiratory tract irritants, people can become "hardened" to the irritation of ammonia and after several exposures can tolerate much higher concentrations than can an unexposed individual.
Under some circumstances, a hardened person can accept an exposure that will result in inflammation of the throat, bronchi, and possibly eyes. An exposure to 300 to 500 ppm for 30 to 60 minutes would cause such an effect and might be hazardous to health.
The current TLV for ammonia is 25 ppm with a short-term exposure limit of 35 ppm. Both were designed to be low enough to cause no irritation in unhardened people. The OSHA PEL for ammonia is 50 ppm, as is the NIOSH Recommended Standard.
The following information about exposure to ammonia gas hazards is based on information from U.S. Army Field Manual 8-285 Chapter 10, Noxious Chemicals:
Ammonia is a colorless gas, soluble in water, with a pungent odor. Liquid ammonia is a vesicant.
Ammonia gas has not been used in warfare but may be encountered in industrial accidents, bombings involving refrigeration plants, and holds of ships as a product of decomposing material.
Exposure to high concentrations of ammonia produces prompt and violent irritation of the eyes and respiratory tract. There may be spasm a nd edema of the glottis or necrosis of the laryngeal mucous membranes. Pulmonary edema may develop and may be complicated by bronchopneumonia.
High concentrations produce violent, burning pain in the eyes and nose, lacrimation, sneezing, pain in the chest, cough, spasm of the glottis, and pulmonary edema. Often there is a temporary reflex cessation of respiration with spasm of the glottis. Edema of the glottis at a later period may seriously interfere with breathing. Concentrations of 0.1 percent are intolerable to humans.
Treatment for ammonia gas exposure consists of prompt removal to pure air and administration of assisted ventilation. Later measures are directed toward the treatment of pulmonary edema, bronchitis, and pneumonia.
The mortality for people exposed to ammonia gas is high following severe exposure. With low concentrations, recovery is usually rapid although bronchitis may persist.
Arsine is arsenic hydride, the combination of arsenic metal and hydrogen gas. Arsine is a water-soluble gas. It is given off whenever freshly-generated hydrogen contacts metallic arsenic especially in an acid environment. As a lead-acid storage battery approaches full charge (in formation or boosting or simply charging), some hydrogen evolves. When arsenic is present in the grids of that battery, some arsine is formed and escapes through the vent caps. If the battery is seriously overcharged, much hydrogen (and arsine if a lead-arsenic alloy is used in the plates) may be given off; an ignition source can then cause the gases to explode.
The main acute effects of arsine on people are lung irritation and hemolysis (destruction of red blood cells). Both effects are usually delayed and do not appear until several hours after the exposure that typically occurs during the acid washing of a tank that has contained an arsenical slag.
Of the two, hemolysis is usually the more serious and is first indicated by pink or red urine that becomes darker with successive voidings. Debris from damaged red cells "clogs up" the kidneys, leading to extremely severe pain and, eventually, to a stoppage of urine flow. Because red cells have been destroyed, severe anemia results so that oxygenation of tissue is impaired. In addition, there may be severe lung irritation (impeding proper oxygenation of blood); death may result from asphyxiation a few days after the exposure.
These effects of arsine are completely avoided if 8-hr exposures are kept at or below 200 ug/cu. m, (0.05 ppm), the TLV and PEL. Whether or not arsine has any chronic effects (such as the causation of cancer) is not known because there has been no study of people or animals chronically exposed to this material.
There are, therefore, no data available indicating that arsine is a carcinogen. Of the three "standards setting" groups, NIOSH is the only one that recommends extremely strict control (2.0 ug/cu. m as determined by 15-min samples) of arsine exposures.
All of the information upon which NIOSH based its Recommended Standard was (and is) available to anyone, including ACGIH and OSHA, of course. If half of the arsine inhaled is excreted in the urine (as seems to be the case for particulate arsenic compounds), then, inhalation of 200 ug/cu. m should result in a urinary concentration on the order of 666 ug/L. Under these circumstances, then, urinary arsenic concentrations might well be useful as indices of arsine exposure/absorption. However, there is very little data in the literature concerning urine concentrations resulting from measured arsine exposures.
Also see ARSENIC IN WATER for more information about arsenic poisoning symptoms and effects.
Bromine is the only halogen that is a liquid at room temperature. Its color is a dark rust red as a liquid and as a gas. As opposed to the "upper respiratory tract" irritants and "lower respiratory tract" irritants, bromine is a "whole respiratory tract" irritant.
That is, its main effects are exerted on the deep lung and may be delayed for some time after the exposure, but it does have far better warning properties than do the lower respiratory tract irritants such as nitrogen dioxide, phosgene, and ozone. Bromine causes eye irritation and lacrimation (tearing) in concentrations below 1 ppm but above the TLV (and PEL) of 0.1 ppm.
Concentrations irritating to the eyes should not be tolerated for more than 15 minutes. Prolonged overexposure to bromine can cause dizziness, headache, and cough followed by abdominal pain and, later, lung edema and pneumonia if the exposure is severe enough. None of these signs/symptoms is at all likely, however, if irritation (eye or respiratory tract) is used as a warning to leave the area of exposure.
The highest TLV (and PEL) assigned to any material is assigned to carbon dioxide, namely 5000 ppm (NIOSH has recommended a Standard of 1.0% or 10 000 ppm for a 10-hr work shift with a ceiling of 3.0% or 30 000 ppm for any 10-min period). Furthermore, these concentrations are far more an expression of good practice than a line between "safe" and "dangerous."
Actually, the concentration of carbon dioxide must be over about 2% (20 000 ppm) before most people are aware of its presence unless the odor of an associated material (auto exhaust or fermenting yeast, for instance) is present at lower concentrations. Above 2%, carbon dioxide may cause a feeling of heaviness in the chest and/or more frequent and deeper respirations. If exposure continues at that level for several hours, minimal "acidosis" (an acid condition of the blood) may occur but more frequently is absent.
As the carbon dioxide concentration climbs above a few percent, the concentration of oxygen in the air inhaled begins to be affected. At 6% carbon dioxide, for instance, the concentration of oxygen in air has decreased from 20.96 to 19.9%. OSHA has indicated that the lowest oxygen concentration for shift-long exposure is 19.5%, corresponding to a carbon dioxide concentration well above 60 000 ppm (6%). Carbon dioxide concentration, not oxygen concentration, is limiting in such circumstances.
Details about Carbon Dioxide Poisoning:See Carbon Dioxide Gas Toxicity hazard levels, poisoning symptoms, & testing. Our CO2 articles include:
Carbon monoxide is a colorless, odorless, tasteless gas that, physiologically, is a chemical asphyxiant. When inhaled, it combines with hemoglobin more readily than does oxygen, displacing oxygen from hemoglobin and thereby interfering with oxygen transport by the blood.
A person suffering from carbon monoxide (CO) intoxication may first experience euphoria (similar to the effect of a martini or two), then headache, followed by nausea and possibly vomiting as the concentration of carboxyhemoglobin in the blood increases.
To prevent these effects, OSHA has established a PEL of 50 ppm for an 8-hr exposure, identical to the TLV. NIOSH, on the other hand, has decided to be more conservative and recommends a standard of 35 ppm. All of these concentrations refer to exposures with durations of 8 hr/day, 40 hr/week for a working lifetime and all are attempts to establish a "no effect" level.
Details about Carbon Monoxide Poisoning:See Carbon Monoxide Gas Toxicity hazard levels, poisoning symptoms, & testing
Our CO articles include:
Hydrogen sulfide (H2S) may be found or produced in buildings from a variety of sources and may be noticed as a sulfur, or rotten egg smell or even as a flatulence odor.
NIOSH Immediately Dangerous To Life or Health Concentration (IDLH): 100 ppm
Potential symptoms: Apnea; coma; convulsions; irritated eyes, conjunctivitis pain, lacrimation, photophobia, corneal vesiculation; respiratory system irritation; dizziness; headaches; fatigue; insomnia; GI disturbances
Health Effects: Acute systemic toxicity (HE4); CNS effects (HE7) Irritation-Eye, (Conjunctivitis), Lungs---Moderate (HE15)
In low concentrations (less than 0.15 mg per liter), hydrogen sulfide may produce inflammation of the eyes, nose, and throat if breathed for periods of 1/2 to 1 hour. Higher concentrations (0.75 mg per liter or greater) are rapidly fatal, presumably by combination of the hydrogen sulfide with the respiratory tissue pigments and the subsequent paralysis of the respiratory center.
The symptoms depend upon the concentration of the gas. At the lowest concentrations, the effects are chiefly on the eyes; that is, conjunctivitis, swollen eyelids, itchiness, smarting, pain, photophobia, and blurring of vision. At higher concentrations, respiratory tract symptoms are more pronounced. Rhinitis, pharyngitis, laryngitis, and bronchitis may occur. Pulmonary edema may result. At very high concentrations, unconsciousness, convulsions, and cessation of respiration rapidly develop.\
Watch out: Higher concentrations of hydrogen sulfide (H2S) gas (0.75 mg per liter or greater) are rapidly fatal, presumably by combination of the hydrogen sulfide with the respiratory tissue pigments and the subsequent paralysis of the respiratory center. - U.S. Army Field Manual 8-285 Chapter 10, Noxious Chemicals
Affected organs: Respiratory system, eyes
Details about hydrogen sulfide sources in buildings are in these articles
(Jan 21, 2016) Garry Boucher said:
What are the health affects of long term exposure (10 years) to Hydrogen Sulphide from a vent pipe which was allowed to vent into a roof cavity. The venting gases, from a septic tank, found their way to bathroom and toilet exhaust vents and contaminated the rooms below those vents.
Please take a look at the Hydrogen Sulfide exposure effects described in the article above. There you will find several links to in-depth articles on just this topic.
Naturally from just your e-text we can't know the level of exposure of individual in the building to the gas you describe.
I'd also look into possible mold and moisture problems in the attic and its insulation .
Please see these articles on methane gas hazards:
The only oxides of nitrogen of concern in most industrial and commercial enterprises are nitric oxide (NO) and nitrogen dioxide (NO2). The main source of both gases is combustion and only under special conditions are appreciable concentrations of nitric oxide formed. Nitric oxide oxidizes in air to nitrogen dioxide which is the more toxic of the two gases.
Nitric oxide, when inhaled, combines with hemoglobin to form nitrosohemoglobin, a carboxyhemoglobin-like material that rather rapidly is oxidized to methemoglobin. That is, its main effect is to inhibit transportation of oxygen
by the blood. Its TLV and PEL are both 25 ppm. Nitrogen dioxide is a deep lung irritant. That is, this gas is not very soluble in water and thus is capable of penetrating deeply into the lung where it undergoes hydrolysis to other materials (acids) that are the actual irritants. Because hydrolysis is a necessary condition for irritation and because hydrolysis takes an appreciable amount of time (several hours in many cases), nitrogen dioxide is known as a delayed-action lung irritant.
Nitric oxide is colorless and may have little or no odor. Nitrogen dioxide (and/or its dimer, nitrogen tetraoxide) is rust red and has a "typical" odor quite notable at 5 ppm and causes eye and nose irritation at 10 to 20 ppm. Currently (1987), the TLV is 3.0 ppm with an STEL of 5.0 ppm; the PEL is 5.0 ppm. NIOSH has recommended 1.0 ppm for a Standard.
The following information about exposure to ammonia gas hazards is based on information from U.S. Army Field Manual 8-285 Chapter 10, Noxious Chemicals:
The term “oxides of
nitrogen” applies to a mixture consisting of nitric
oxide, nitrogen dioxide, and nitrogen tetroxide. Nitric
oxide is colorless. The other oxides are red-brown
(1) The danger of nitrous fume poisoning is or cordite) are burned or detonated in poorly ventilation areas. This may occur in gun pits, armored vehicles, ship magazines, and turrets. This may also occur in mining and tunneling operations.
(2) In addition, nitrous fumes are emitted from fuming nitric acids (white and red) and are generated by the combustion of certain plastics.
Watch out: improper use of ozone generators to try to kill mold or odors may oxidize certain common plastics found in buildings, leading to the hazards discussed here. [OPINION-DF].
See OZONE HAZARDS
Inhalation of nitric oxide causes the formation of methemoglobin and does not appear to lead to any tissue lesions. Inhalation of nitrogen dioxide results in the formation of nitrite that leads to a fall in blood pressure and to the production of methemoglobin. Inhalation of high concentrations of nitrogen dioxide (above 0.5 mg per liter) causes rapid death without the formation of pulmonary edema.
Somewhat lower concentrations of nitrogen oxide gas exposure result in death with the production of yellow, frothy fluid in the nasal passages, mouth, and trachea and marked pulmonary edema. The findings in other tissues are negligible.
The symptoms following inhalation of nitrous fumes are due chiefly to nitrogen dioxide. The symptoms presented depend upon the concentration of the gas. Exposures to higher concentrations cause severe local irritation with choking and burning in the chest, violent coughing, yellow staining of the mucous membranes, expectoration of yellow-colored sputum, headache, and vomiting.
Often, these early symptoms may be mild or entirely absent. After 2 to 24 hours, symptoms start with coughing, nausea, vomiting, frothy sputum, dyspnea, cyanosis, convulsions, and signs of lung edema. This train of symptoms may result in death.
At nitrogen gas exposures to very high concentrations for short periods of time, the onset of symptoms is very sudden and marked. Convulsions, unconsciousness, and respiratory arrest occur within a short time and death may follow rapidly.
The diagnosis is made from the history, symptoms described, and sometimes the pungent odor of the gas or the yellow discoloration of the exposed mucous membranes.
Treatment of casualties with symptoms of pulmonary irritation is the same as for CG poisoning (chap 5).
The few cases with symptoms referable to the CNS either die quickly or, on removal to fresh air, recover spontaneously. Fatal cases usually die within 48 hours. Bronchopneumonia and varying degrees of pulmonary fibrosis and emphysema often follow recovery from the acute stage.
Nitrogen Oxides: Air Quality Criteria for Oxides of Nitrogen, Vol III of III, US EPA, EPA600/8-91/049cF, August 1993, web search 08/28/2010, original source: http://nepis.epa.gov [Large PDF 25MB]
Key chapters in this document evaluate the latest scientific data on (a) health effects of NOx measured ill laboratory animals and exposed human populatIOns and (b) effects of NOx on agricultural crops, forests, and ecosystems, as well as (c) NOx effects on visibility and nonbiological materials.
Other chapters describe the nature, sources, distribution, measurement, and concentratiOns of NOx m the environment These chapters were prepared and peer revived by experts from various state and Federal government offices, academia, and private industry for use by EPA to support decision makIng regarding potentIal risks to public health and the enVIronment Although the document IS not intended to be an exhaustIve literature reVIew, It IS intended to cover all the pertinent literature through early 1993
Ozone is a kind (called an "allotrope") of oxygen . It is formed in the ionosphere by the action of ultraviolet radiation from sunlight on oxygen. Lightning strokes are another natural source of ozone and the characteristic odor of that material can often be noted during and after a thunderstorm.
When pollutants are emitted into the air either by man or nature, almost all are eventually removed by one or more of several processes including reaction under the influence of ultraviolet radiation. One series of such reactions results in the formation of ozone as a "secondary" (formed by reaction in the air) air pollutant, often in rather high concentrations (several tenths of a part per million).
As ozone can be formed by nature's sparks (lightning), it can also be formed by man's. Whenever an electrical spark or corona occurs in air, some ozone is formed. This accounts for the characteristic odor noted near an operating electric motor such as an electric shaver.
Because ozone is found in so many places, its toxicity (ability to injure a living organism by other than mechanical means) has been investigated extensively since the early 1900s. Experimentation has shown that the odor of ozone can be detected and identified by most people at a concentration of from 0.02 to 0.05 ppm (parts ozone per million parts air + ozone). As the concentration increases to a few tenths of a part per million, the first effect noted is likely to be a feeling of dryness in the back of the throat. If a concentration on the order of 0.2 or 0.3 ppm is inhaled more or less continuously for several hours to a few days some lung irritation may result.
Higher concentrations of ozone can produce several kinds of toxic effects if exposures are sufficiently prolonged. Eye irritation (despite newspaper and TV accounts seemingly indicating otherwise) occurs only at concentrations high enough to result in other, more severe, toxic effects.
Ozone is a very reactive substance. It will readily react with just about any material capable of being oxidized, and with many that are not. The material with which it reacts may be a gas or vapor, a particle floating in the air (a mold spore, for example), or a solid (or liquid) surface. For this reason, when ozone is present in most enclosed spaces its concentration declines quite rapidly with time. Of course, if ozone is being generated more rapidly than it is destroyed by reaction, its concentration can build up. This is the main reason why devices that produce relatively large amounts of ozone are safe only in relatively large enclosures and why the ozone generation rate should be reduced in small enclosures.
Ozone is well known for its ability to eliminate certain odors. How this is accomplished is controversial. At concentrations just above the odor threshold, some odors do seem to vanish. The main reason for this may be ozone's ability to desensitize the olfactory apparatus so that the odors can no longer be perceived.
Some evidence indicates that this may be the case at least occasionally. Other evidence indicates that ozone may react with the odor-causing substances, eliminating them from the air (this is probably the only mechanism that operates when concentrations are below the odor threshold).
Finally, some people have insisted that even if ozone does not paralyze the olfactory sense, its odor is such that it "masks" other odors. Perhaps all three mechanisms operate, each in its own area of effectiveness. As with all other materials, ozone has a dose-effect relationship with a threshold. That is, once the threshold dose has been exceeded, toxic effects are proportional to dose.
For inhaled gases, dose is proportional to both time and concentration. If the duration of exposures cannot be controlled (as is usually the case), then the concentration must be kept low enough so that no injury will occur even from prolonged and repeated exposures.
For ozone, that "threshold" concentration is 0.1 ppm. So long as concentrations are kept at or below that level, injury is not expected even in the most sensitive workers so long as their exposure durations coincide reasonably well with or are less than the 8 hr/day, 40 hr/wk regimen. This "threshold" level is accepted by the American Conference of Government al Industrial Hygienists (and is called the Threshold Limit Value by that organization) and by the Occupational Safety and Health Administration, OSHA.
The TLV or OSHA's Permissible Exposure Level (PEL) is not a fine line between safe and non-safe. Instead, it represents the best judgment of a group of experts of the highest concentration that can be inhaled repeatedly by a population of workers with no resulting injury. Higher concentrations may or may not have any particular effect on a specific individual.
Ozone is a highly toxic gas but even highly toxic substances can be encountered safely. The main concern with this material is that concentrations to which people are exposed do not average more than 0.1 ppm over an 8-hr day, and do not exceed that value by more than a factor of 2 or 3 during the exposure.
See OZONE WARNINGS - Use of Ozone as a "mold" remedy is ineffective and may be dangerous.
Our complete list of articles about ozone can be found at OZONE HAZARDS - home
Please see details at PROPANE GAS EXPOSURE EFFECTS - separate article
The greatest LP gas or propane gas exposure risk other than fire or explosion, would be not the exposure to LP gas or propane gas itself but the prolonged absence of sufficient oxygen if someone is enclosed in a space with high concentration of propane. No long term exposure health risks associated with LP gas or propane have been reported at low concentrations.
Propylene is a simple asphyxiant (that is, it acts by dilution of oxygen) and a rather poor anesthetic. Extremely high concentrations are required to produce any effect at all.
No TLV or PEL has ever been established for this material and NIOSH has not recommended a Standard. Its lower explosive limit is 2% in air (the upper is 11.1%) and a reasonable value for a maximum permissible concentration (suggested by Gerarde in Patty's Industrial Hygiene and Toxicology, vol 2, p. 1204, Interscience, New York, 1963) is 1/5 of the LEL or 4000 ppm.
14 March 2016 Sarah said:
Is refrigerant leakage dangerous in any way?
This question was posted originally at REFRIGERANT DIAGNOSTIC FAQS
Yes, Sarah, refrigerant gases can be fatal, though the probability of a fatal exposure level of refrigerant gas in a home from a home appliance is probably close to zero - there's not that much refrigerant gas in a typical home appliance.
Here are the details: While refrigerant gases are rather inert and non-toxic, they can replace oxygen. As a result, if you were in a very small space inside which the concentration or level of refrigerant gas became too high, you might not sense any problem but you could become asphyxiated by lack of oxygen - a condition referred-to as anoxia. Such cases are rare but possible.
Below I cite research confirming that the risks of fatality from high concentrations of refrigerant gases are not just theory. These hazards have been understood at least since the 1930's and probably earlier.
See SULPHUR DIOXIDE GAS TOXICITY for details. For sulfur dioxide, the TLV had been 5.0 ppm for many years, but in 1978 ACGIH announced its intention to reduce that TLV to 2.0 ppm; that was done in 1980.
Continue reading at GAS EXPOSURE LIMITS & STANDARDS or select a topic from closely-related articles below, or see our complete INDEX to RELATED ARTICLES below.
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(Oct 20, 2015) Kay Quinn said:
I have been stalked for 4 months. In the last 3 weeks an odor has appeared in the house that causes headaches and vomiting. Can this detect if I am being poisoned?
You first need to take this concern to your doctor. If she agrees that indoor environment conditions could be causing your symptoms you need an onsite expert to inspect and if appropriate test your home for possible causes. If your doctor believes it's appropriate, then an industrial hygienist familiar with residential hazards of a similar environmental inspector might be found at CONSULTANTS & EXPERTS DIRECTORIES
To address your concern about being stalked, you should call your local police department for help and advice.
(Oct 23, 2016) Jill said:
My family & I have been sick for 2 months. My 10yr old daughter has suffered far more than the rest of us. No one could diagnosis her. Her eyes hurt,her body hurt,she had bubbles throughout her body & vibrations.
Throat pain,choking sensation, & the feeling of someone sitting on her. She was getting rashes & finally a doctor tested her for pneumonia. It came back positive. The day of her last dose her symptoms came back with a vengeance. Her eyes were way more painful, had floaters,flashes of lights/stars,on & on.
Doctors said anxiety. I began to get sick during all of this & thought anxiety for myself. My heart raced. Had chest pain & it worsened with activity. I began to think mold. My husband said maybe carbon monoxide. So I had the gas company out because we have since moving in,smelled poo. Gas company found nothing. My husband has a meter that was picking up combustible gases so I called public utilities out. His meter didn't & told me I was paranoid. So my husband called a plumber friend. He said to run water through the vents for sewer gas. 1st one nothing. 2nd one drenched me. C
alled fire department & they said get out. Landlord is a weird guy. He came out though & knew exactly where to cut to fix the pipe. It was severed in half. We've been living in this house for 2 months & I homeschool so we rarely leave. The next day we returned to the house but immediately began feeling the same pain & symptoms. We could still smell it too but th e meter wasn't picking it up. Oh-I found an neuro-ophthalmologist right before we had the discovery & she said my daughter has a traumatic brain injury. She said it can be caused by methane/carbon monoxide/gases poisoning. My lungs burn. Xray was clear but I hurt so much.
Questions: can the poisons stay in the walls/items even after the pipe was repaired? CDC seems to think so. And, seeing I am & my daughter is still experiencing symptoms after leaving, does it mean it's chronic? We are going to a neurologist but I know my lungs hurt so bad. She had bubbles that make me think that she had venous air embolism. I feel so blessed none of us died. The sewer pipe was completely cut in half. My other 2 children also have symptoms similar to ours but are a little less severe. None of our symptoms are getting better even after a few days away. Like I said as soon as we reentered,it hit us so hard we had to leave.
Thanks for any help.
No one can safely diagnose a serious indoor environmental hazard simply by reviewing text. You need an on-site expert.
However I can say that in my opinion gases are not likely to remain long-term in a building once the gas Source has been found and corrected. I should add a, however, that if there was a sewage leak or if there was another source of mold or indoor pathogens or contaminants such as particles or chemicals, those could remain in the building even after the original source has been removed. For example a sewage backup could leave hazardous bacteria and other pathogens and even hazardous heavy metals in the building.
The fact remains If You observe a strong odor as soon as you enter a building then almost certainly there's a source that has not been found and corrected.
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