By Y. Avogadro. Mars Hill College. 2018.
A4th Ebola subtype buy xalatan 2.5 ml with mastercard, Reston cheap 2.5 ml xalatan, causes fatal hemorrhagic disease in nonhu- man primates originated from the Philippines in Asia; few human infec- tions have been documented and those were clinically asymptomatic discount xalatan 2.5 ml visa. A new subtype of Ebola virus was recovered from one person probably infected while dissecting an infected chimpanzee in Coˆte-d’Ivoire in 1994 buy generic xalatan 2.5 ml on-line. In 1995, a major Ebola outbreak with 315 cases and 244 deaths was centered on Kikwit (Democratic Republic of the Congo, formerly Zaire). Between the end of 1994 and the third trimester of 1996 three outbreaks reported in Gabon resulted in 150 cases and 98 deaths. Between August 2000 and January 2001 an epidemic (425 cases, 224 deaths) occurred in northern Uganda. From October 2001 to April 2003, several outbreaks were reported in Gabon and the Republic of Congo with a total of 278 cases and 235 deaths; high numbers of deaths were reported among wild animals in the region, particularly non-human primates. Antibodies have been found in residents of other areas of sub-Saharan Africa; their relation to the Ebola virus is unknown. End 2003, an outbreak in the Republic of Congo, with high case-fatality and thought to be related to contact with non-human primates, was rapidly controlled. In Reston, 4 animal handlers with daily exposure to these monkeys in 1989 developed speciﬁc antibodies. Marburg disease has been recognized on 5 occasions: in 1967, in Germany and what was then the Federal Republic of Yugoslavia, 31 humans (7 fatalities) were infected following exposure to African green monkeys (Cercopithecus aethiops) imported from Uganda; in 1975, the fatal index case of 3 cases diagnosed in South Africa had been infected in Zimbabwe; in 1980, 2 linked cases, 1 of which fatal, were conﬁrmed in Kenya; in 1987, a fatal case occurred in Kenya. From 1998 to 2000, in the Democratic Republic of the Congo, at least 12 cases were conﬁrmed among more than 145 suspected cases (case-fatality rate 80%) of Marburg viral hemorrhagic fever. In Africa, Ebola infections of human index cases were linked to contact with gorillas, chimpanzees, monkeys, forest duikers and porcupines found dead or killed in the rainforest. So far, Ebola virus has been detected in the wild in carcases of chimpanzees (in Coˆte-d’Ivoire and Republic of Congo), gorillas (Gabon and Republic of Congo) and duikers (Republic of Congo), found dead in the rainforest. Person-to-person transmission occurs through direct contact with infected blood, secretions, organs or semen. Risk is highest during the late stages of illness when the patient is vomiting, having diarrhea or hemorrhaging, and during funerals with unprotected body preparation. Under natural conditions, airborne transmission among humans has not been documented. Nosocomial infections have been frequent; virtually all patients who acquired infection from contaminated syringes and needles died. Period of communicability—Not before the febrile phase and increasing with stages of illness, as long as blood and secretions contain virus. Ebola virus was isolated from the seminal ﬂuid on the 61st, but not on the 76th, day after onset of illness in a laboratory acquired case. Methods of control—No vaccine and no speciﬁc treatment avail- able as yet for either Ebola or Marburg. See control measures for Lassa fever: 9B, C, D and E; plus protection of sexual intercourse for 3 months or until semen can be shown to be free of virus. Cysts usually develop in the liver but also in other viscera, nervous tissue or bone. Identiﬁcation—Larval stages of the tapeworm Echinococcus granulosus, the most common Echinococcus, cause cystic echinococcosis or hydatid disease. Infections may be asymptomatic until cysts cause notice- able mass effect; signs and symptoms will vary according to location, cyst size, cyst type and numbers. Ruptured or leaking cysts can cause severe anaphylactoid reactions and may release protoscolices that can produce secondary echinococcosis. Cysts are typically spherical, thick-walled and unilocular, most frequently found in the liver and lungs, although they may occur in other organs. Clinical diagnosis is based on signs and symptoms compatible with a slowly growing tumour, a history of residence in an endemic area, along with association with canines. Differential diagnoses include malignancies, amoebic abscesses, congenital cysts and tuberculosis. Radiography, com- puterized tomography and sonography along with serological testing are useful for laboratory diagnosis. Deﬁnitive diagnosis in seronegative patients, however, requires microscopic identiﬁcation from specimens obtained at surgery or by percutaneous aspiration; the potential risks of this (anaphylaxis, spillage) can be avoided by ultrasound guidance and anthelmintic cover- age. Species identiﬁcation is based on ﬁnding thick laminated cyst walls and protoscolices as well as on the structure and measurements of protoscolex hooks. Infectious agent—Echinococcus granulosus, a small tapeworm of dogs and other canids. Occurrence—All continents except Antarctica; depends on close association of humans and infected dogs. Especially common in grazing countries where dogs consume viscera containing cysts. Control programs exist in Argentina, Brazil, China, Kenya (Turkana district), Spain, Uruguay and other countries, including those of the Mediterranean basin. Felines and most other carnivores are normally not suitable hosts for the parasite. Intermediate hosts include herbivores, primarily sheep, cattle, goats, pigs, horses, camels and other animals. Mode of transmission—Human infection often takes place during childhood, directly with hand-to-mouth transfer of eggs after association with infected dogs or indirectly through contaminated food, water, soil or fomites. Adult worms in the small intestines of canines produce eggs containing infective embryos (oncospheres); these are passed in feces and may survive for several months in pastures or gardens. When ingested by susceptible intermediate hosts, including humans, eggs hatch, releasing oncospheres that migrate through the mucosa and are bloodborne to organs, primarily the liver (ﬁrst ﬁlter), then the lungs (second ﬁlter), where they form cysts. Sheep and other intermediate hosts are infected while grazing in areas contaminated with dog feces containing parasite eggs. Incubation period—12 months to years, depending on number and location of cysts and how rapidly they grow. Period of communicability—Not directly transmitted from per- son to person or from one intermediate host to another. Most canine infections resolve spontaneously by 6 months; adult worms may survive up to 2 3 years. Susceptibility—Children, who are more likely to have close con- tact with infected dogs and less likely to have adequate hygienic habits, are at greater risk of infection, especially in rural areas. Preventive measures: 1) Educate those at risk on avoidance of exposure to dog feces. Emphasize basic hygiene practices such as handwashing, washing fruits and vegetables and control of contacts with infected dogs. Eliminate ownerless dogs whenever possible and encourage responsible dog owner- ship. Control of patient, contacts and the immediate environment: 1) Report to the local health authority: Not normally a report- able disease, Class 3 (see Reporting). Chemotherapy with mebendazole and albendazole has proved successful and may be the preferred treatment in many cases. If a primary cyst ruptures, praziquantel, a protoscolicidal agent, reduces the probability of secondary cysts. Epidemic measures: In hyperendemic areas, control popula- tions of wild and ownerless dogs.
The presence of long history of respiratory disease sug- gests chronic lung disease discount 2.5 ml xalatan mastercard. On the other hand order 2.5 ml xalatan, developing cyanosis without exacer- bation of respiratory symptoms suggests etiologies other than lung disease buy 2.5 ml xalatan otc. Long-standing congenital heart disease causing increase in pulmonary blood flow with eventual damage to the pulmonary vasculature is a likely cause of this patient’s symptoms and signs order xalatan 2.5 ml on-line. Pulmonary arterial systolic pressure was measured through a tricuspid regurgitation jet which indicates a right ventricular/ pulmonary arterial systolic pressure of about 100 mmHg. This gentleman has a large atrial septal defect with pulmonary vas- cular obstructive disease due to long standing increase in pulmonary blood flow. The high pulmonary blood flow caused pulmonary congestion during childhood 102 Ra-id Abdulla and A. However, with unrepaired lesions, there is likelihood that pulmonary vascular obstructive disease progress causing the pulmonary vascular disease to be significantly elevated, leading to right to left shunting at the atrial septal defect resulting in cyanosis. If reversible, then closure with ongoing management of pulmo- nary vascular obstructive disease can be considered. Otherwise, the only alternative available is the chronic use of pulmonary vascular dilation therapy such as oxygen, sildenafil, bosentan, and intravenous agents such as continuous prostacyclin infusion. Khalid and Ra-id Abdulla Key Facts • Children with ventricular septal defects are typically asymptomatic. The ventricular septum is normally a solid wall completely sepa- rating the 2 ventricles. Khalid (*) Children’s Heart Institute, Mary Washington Hospital, 1101 Sam Perry Blvd. Khalid and Ra-id Abdulla Incidence Ventricular septal defect is the most common cardiac defect, and it accounts for 15–20% of all cardiac defects. The incidence of ventricular septal defect is slightly more common in females (56%). Pathology The ventricular septum can be divided into a small membranous region and a much larger muscular septum; the latter makes up the bulk of the ventricular septum and can be further divided into an inlet, trabecular, and outlet regions. Ventricular septal defects may occur in any part of the ventricular septum, it may be single or multiple, and it may also be associated with other forms of congenital heart defects. The ven- tricular septal defect is usually classified by its location in the ventricular septum. The defect occurs in the membranous septum and involves some of the surrounding tissue, thus sometimes called perimembrenous or paramembranous defect (Fig. A defect in and around the membranous region of the ventricular septum is known as perimembrenous ventricular septal defect (sometimes referred to as paramembrenous). It is located beneath the tricuspid valve, posterior, and inferior of the membranous septum. Muscular ventricular septal defect accounts for 5–20% of all ventricular septal defects. Outlet (infundibular, conal, and supracristal) ventricular septal defect account for 5–7% of all types of defects. The defect is located in the outlet septum, beneath both semilunar (pulmonary and aortic) valves. Pathophysiology The magnitude of shunting from one chamber to the other depends on the size of the defect and the difference between the systemic and pulmonary vascular resistance. In small ventricular septal defects the defect is restrictive and the amount of shunting will be hemodynamically insignificant. If the defect is large there will be significant shunting to the right side depending primarily on the difference between the systemic and pulmonary vascular resistance (Fig. The pulmonary vascular resistance is significantly less than the systemic vascular resis- tance, therefore, any abnormal communication between the left and right sides of the heart will result in left to right shunting. Blood flow to the lungs versus that to the body (Qp:Qs ratio) in this scenario is 6:2 or 3:1 106 O. Khalid and Ra-id Abdulla of the pulmonary arteries, left atrium, and left ventricle. The excessive shunting will also cause increase in pulmonary blood flow and congestive heart failure sec- ondary to volume overload. Pulmonary congestion will lead to respiratory symp- toms, recurrent respiratory infections, and feeding difficulties. Significant left to right shunting will cause decrease in the systemic cardiac output manifested by exercise intolerance, diaphoresis, poor feeding, and failure to thrive. The pulmo- nary vascular resistance is high in the newborn period, and the left to right shunting will not be significant, therefore the infant is typically asymptomatic in the first 2 months of life, with no significant heart murmur in the first few days of life. With a large (unrestrictive) ventricular septal defect, the right ventricle and the pulmonary vascular bed will be facing systemic pressures; if left untreated, this may cause an irreversible change in the pulmonary arterioles causing pulmonary vascular obstructive disease (Eisenmenger’s syndrome) with subsequent right to left shunting and cyanosis. This complication is delayed according to the size of the defect; large defects may cause irreversible changes in the pulmonary vasculature during early childhood. Blood shunting in a turbulent fashion across the ventricular septal defect may affect adjacent structures such as the aortic valve leading to prolapse of the aortic cusp closer to the defect and this may progress to aortic valve regurgita- tion. If left untreated, it may cause left ventricular dilatation and worsening heart failure. Clinical Manifestations Most infants with small ventricular septal defects are asymptomatic. The heart murmur may not be detected at birth due to the high pulmonary vascular resistance and low pressure difference between right and left ventricles. As the pulmonary vascular resistance drops, the left to right shunting across the defect will increase and become more turbulent resulting in a heart murmur. In moderate to large ventricular septal defect, the infants present with symptoms secondary to increased pulmonary blood flow (pulmonary edema) and decrease in cardiac output such as tachypnea, increased respiratory effort, recurrent pulmonary infections, poor feeding, diapho- resis, easy fatigability, and failure to thrive. Older patients may present with heart failure, hemoptysis, arrhythmia, cyanosis, or bacterial endocarditis. On examination, infants with small or moderate ventricular septal defects usu- ally present only with holosystolic murmur (Fig. In large ventricular septal defects, infants are often tachypneic with failure to thrive and show signs of conges- tive heart failure such as respiratory distress (respiratory retraction and nasal flar- ing), and an enlarged liver. A systolic thrill may be palpable in small or medium ventricular 7 Ventricular Septal Defect 107 Fig. The intensity of S1 is diminished by the onset of the heart murmur; S2 is normal in small ventricular septal defects, but it increases in intensity in mod- erate ventricular septal defect; S2 is loud and single in patients with pulmonary hypertension. Frequently, secondary to the holosystolic murmur, S1 and S2 are masked by the murmur spanning the entire duration of systole. Ventricular septal defect murmurs may be 2–5/6 in intensity and harsh in quality, it is best heard over the left lower sternal border. A mid-diastolic rumble at the apical region is often heard in large ventricular septal defects due to the increased flow across the mitral valve. The degree of cardiomegaly and increased vascular markings is proportional to the amount of left to right shunting. In pulmo- nary vascular obstructive disease, the cardiac size is normal with no evidence of increase in pulmonary vascular markings, but the pulmonary artery segment at the mid left border of the cardiac silhouette may be more prominent. Left atrial dilatation and left ventricular hypertrophy may be seen in moderate ventricular septal defect.
Laboratory tests Histopathological examination of skin lesions generic 2.5 ml xalatan, blood examination (leukocytosis with neutrophilia) best 2.5 ml xalatan. Staphylococcal Infection Definition Staphylococcal infection is a rare infection of the oral mu- cosa xalatan 2.5 ml low cost. Etiology Staphylococcus aureus and Staphylococcus epidermides are the most causative strains buy xalatan 2.5 ml visa. Predisposing factors are trauma of the oral mu- cosa, poor oral hygiene, and systemic diseases such as diabetes mellitus, tuberculosis, immune deficiencies, and congenital neutropenia. Clinical features Staphylococcal oral infection appears as a round or oval, abnormal, solitary ulcer with raised inflammatory border. The sur- face of the ulcer is covered by a whitish or yellow-white necrotic exudate (Fig. Laboratory tests The definite diagnosis requires isolation of Staph- ylococcus species fromsmear and cultures. Differential diagnosis Streptococcal infection, aphthous ulcer, me- chanical trauma, chancre, tuberculous ulcer, cyclic neutropenia, myelo- dysplastic syndromes, Wegener granulomatosis. Usage subject to terms and conditions of license 196 Ulcerative Lesions Congenital Neutropenia Definition Congenital neutropenia is a rare hematological disorder characterized by a quantitative persistent decrease of neutrophils in the peripheral blood associated with life-threatening bacterial infec- tions. Both autosomal dominant and recessive transmis- sion have been reported, but some cases appear to be sporadic. Clinical features The main clinical manifestations are recurrent infec- tions, which are usually present at birth. The most common infections involve the respiratory and urinary tracts, middle ear, skin, and oral mucosa. Oral lesions are common and present as persistent and recur- rent ulcerations, which may lead to scar formation (Fig. Gingivitis and severe ag- gressive periodontitis, leading to tooth mobility, are common. Af- fected children tend to improve with age and some undergo total re- mission in late childhood. Differential diagnosis Cyclic neutropenia, agranulocytosis, leukemia, glycogen storage disease type Ib, Chédiak–Higashi syndrome, hypophos- phatasia, acatalasia, aggressive periodontitis. Treatment A high level of oral hygiene, periodontal treatment, sys- temic antibiotics. Cytomegalovirus Infection Definition Oral infection with cytomegalovirus is a relatively rare dis- order. Clinically, it presents as nonspecific painful ulcerations, usually on the gingiva and tongue (Fig. Laboratory tests Histopathological examination, immunochemistry, and molecular biology tests. Differential diagnosis Aphthous ulcers, herpetic stomatitis, drug-re- lated ulceration, mechanical trauma. Usage subject to terms and conditions of license 199 6 Papillary Lesions Papillary lesions of the oral mucosa are a small group, appearing clin- ically as exophytic growths with a verrucous or cauliflower-like surface. Reactive lesions, benign tumors, malignancies, and systemic diseases are included in this group. O Papilloma O Focal epithelial hyperplasia O Condyloma acuminatum O Epulis fissuratum O Verruca vulgaris O Crohn disease O Verruciformxanthoma O Acanthosis nigricans, malig- O Verrucous carcinoma nant O Squamous-cell carcinoma O Familial acanthosis nigricans O Verrucous leukoplakia O Darier disease Laskaris, Pocket Atlas of Oral Diseases © 2006 Thieme All rights reserved. Usage subject to terms and conditions of license 200 Papillary Lesions Papilloma Papilloma is a common benign proliferation, originating from the strati- fied squamous epithelium (see also p. Clinically, papilloma presents as a painless, exophytic, well-circumscribed and usually pedunculated lesion. Typically, it consists of numerous fingerlike projections, which give the lesion a “cauliflower” appearance (Fig. The differential diagnosis includes verruca vulgaris, con- dyloma acuminatum, early verrucous carcinoma, and verruciform xan- thoma. Usage subject to terms and conditions of license 202 Papillary Lesions Condyloma Acuminatum Definition Condyloma acuminatum is a sexually transmitted benign lesion, mainly occurring in the anogenital region, and rarely in the mouth. Clinical features Oral lesions appear as single, or more often multiple, small, sessile, well-demarcated, exophytic masses with a cauliflower-like surface (Fig. The lesions have a whitish or normal color, and usually recur; the average size is 0. The labial mucosa, tongue, gingiva, buccal mucosa, and soft palate are the sites most frequently affected. The anogenital lesions present as discrete or multiple, sessile or pedunculated, exophytic, small nodules with cauliflower-like appearance. The lesions may have whitish or brownish color and size that varies from1–5 mm to several centimeters in diameter. Differential diagnosis Papilloma, verruca vulgaris, focal epithelial hy- perplasia, verruciform xanthoma, sialadenoma papilliferum, focal der- mal hypoplasia syndrome, early verrucous carcinoma, molluscum con- tagiosum. Usage subject to terms and conditions of license 204 Papillary Lesions Verruca Vulgaris Definition Verruca vulgaris, or common wart, is a benign, mainly cutaneous lesion that may rarely appear in the oral mucosa. Fromthe skin lesions, the virus can be autoinoculated into the oral mucosa, usually on the vermilion border and the lip mucosa, com- missures, and tongue. Clinically, it appears as a painless, small, sessile, and well-defined exophytic growth with a cauliflower surface and whit- ish color (Figs. Differential diagnosis Papilloma, condyloma acuminatum, verruci- formxanthoma, focal epithelial hyperplasia. Usage subject to terms and conditions of license 206 Papillary Lesions Verruciform Xanthoma Definition Verruciformxanthoma is a rare hyperplastic disorder of the oral mucosa. Typically, it appears as a well-demarcated, painless, sessile, slightly elevated lesion. Differential diagnosis Papilloma, verruca vulgaris, condyloma acumi- natum, sialadenoma papilliferum, verrucous carcinoma. Typically, it presents as an exophytic, whitish mass with a papillary or verruciformsurface (Fig. Along with the clinical fea- tures, biopsy and histopathological examination should be performed to rule out other papillary growths. Verrucous carcinoma is well-differ- entiated, slow-growing, rarely metastasizes, and has a good prognosis. Usage subject to terms and conditions of license 208 Papillary Lesions Squamous-Cell Carcinoma Squamous-cell carcinoma has a wide range of clinical presentations (see also pp. It has a papillary or verruciformsurface and a red, whitish, or normal color (Fig. The surface is usually ulcerated, and the base of the lesion is indurated on palpation. The buccal mucosa, tongue, floor of the mouth, and gingiva are the most common regions affected by this clinical form of carcinoma. Verrucous Leukoplakia Verrucous leukoplakia is a rare clinical formof leukoplakia with a greater risk of malignant transformation (see also p. Clinically, it presents as an irregular, white, exophytic plaque with a papillary surface (Figs. Verrucous leukoplakia occurs more frequently in women (the female to male ratio is about 4 : 1).
They come out of their metacercarial cyst as a small adult and quickly attach themselves to the intestine with a sucker cheap xalatan 2.5 ml with mastercard. Four common flukes are: human intestinal fluke xalatan 2.5 ml mastercard, human liver fluke purchase xalatan 2.5 ml visa, sheep liver fluke purchase 2.5 ml xalatan free shipping, pancreatic fluke of cattle. Has cilia, can swim vigorously and must find intermediate snail host in one to two hours or may be too exhausted to in- vade. Those are "mother" redia, and each one bears "daughter" redia for up to 8 months, all still inside the snail, and living on the fluids in the lymphatic spaces. If the snail is feeding on a plant, cercaria can latch onto plant with sucker mouth and start to encyst (form a "cocoon") within minutes. But as you eat the plant it is stuck to, the least pressure will break it, leaving the cyst in the mouth. The "almost unbreakable" inner cyst wall protects it from chewing, and the keratin-like coat prevents digestion by stomach juices. However when it reaches the duodenum, contact with intestinal juices dissolves away the cyst-wall and frees it. It then fastens itself to the intestinal lining and begins to develop into an adult. Note that the adult is the only stage that “normally” lives in the human (and then only in the intestine). Fasciolopsis depends on a snail, called a secondary host, for part of its life cycle. If propyl alcohol is the solvent, the intestinal fluke is invited to use another organ as a secondary host—this organ will become cancerous. If xylene (or toluene) are the solvents, I typically see any of four flukes using the brain as a secondary host. I call the diseases caused by fluke stages in inappropriate locations Fluke Disease; it is discussed in more detail later (page 249). Pollutants can invade your body via the air you breath, the foods and beverages you eat, and the products you put on your skin. The one who did not assumes the cream is not harmful to them…that they are like a bank vault, impreg- nable to that product. A better assumption is that the face cream is somewhat toxic, as evidenced by the rash that can develop, and they escaped the rash only because they had a stronger im- mune system. The immune system is like money, paid out of the bank vault, for every toxic invasion. Most other solvents dissolve fats and are life threatening, because fats form the membrane wall around each of our cells, especially our nerve cells. Metal Pollution Biochemists know that a mineral in raw element form always inhibits the enzyme using that mineral. Inorganic copper, like you would get from a copper bottomed kettle or copper plumbing, is 3 carcinogenic. We put metal jewelry on our skin, eat bread baked in metal pans, and drink water from metal plumbing. Mercury amalgam fillings, despite the assurances of the American Dental Association, are not safe. And sometimes the mercury is polluted with thallium, even more toxic than mercury! Gold and silver seem to have fewer harmful effects, but no one should have any pure metal in or on their body. Other prevalent toxic metals include lead and cadmium from soldered and galvanized plumbing, nickel and chromium from dentalware and cosmetics, and aluminum from food and drink cans, and cooking pots. From Carcinogenicity and Metal Ions, volume 10, page 61, of a series called Metal Ions in Biological Systems, edited by Helmut Sigel, 1980. One small moldy fruit or vegetable can pol- lute a huge batch of juice, jam or other product. Although molds are alive, and can be killed by zapping, mycotoxins are not, and must be detoxified by your liver. But because mycotoxins are so extremely poisonous, a tiny amount can incapacitate a part of the liver for days! For that reason I am always cautioning people to eat only perfect citrus fruit, and never drink commercial fruit juice. Of the thousands of oranges that go into the batch of orange juice you drink, one is sure to be moldy, and that is all it takes to give your liver a setback. It also helps get rid of aflatoxin before it is consumed, right in the food container. So keep a plastic shaker of vitamin C powder handy and use it like salt on all your food. Physical Toxins Breathing in dust is quite bad for you so your body rejects it by sneezing, coughing, spitting up and out. But because it is sharp it gets caught in your tissue, then works its way deeper and deeper. We are unaware that it fills our homes when fiberglass insulation is left imperfectly sealed off. Any hole made through the ceiling or wall, even if covered with cloth, lets swarms of broken glass bits into the house air. Of course, fiberglass should never be used in home construction, draperies, or around water heaters. The best advice is to have it all removed while you are away and then vacuum and dust. Chronic exposure from a single small hole in the ceiling does a lot of harm, leading to cyst formation. And that cyst is a perfect place for parasites and bacteria to settle and multiply. Asbestos is another tiny bit, sharp as glass, that moves through your body like a swordfish, impaling your cells until it, too, gets routed into a cyst. We have been led to believe that we no longer have asbestos in our homes because we have outlawed the fireproofing mate- rials it was used in. While that may be true, the source I find most often is all too prevalent: the clothes dryer belt. As it gets hot the belt releases a blast of asbestos particles that are forced through the seams of your dryer, and also openings in your exhaust hose, by the high pressure formed inside. By the time your air conditioner or refrigerator needs recharging, you have been exposed for a long time. Our diligent scientists have studied the mechanism of arsenic poisoning in great detail. Then why are we allowed to put it on our lawns to be carried into our carpets via shoes? As a result, foam fur- niture, pillows and mattresses give off formaldehyde for about two years after manufacturing.
10 of 10 - Review by Y. Avogadro
Votes: 275 votes
Total customer reviews: 275