Worker as a teacher of glass painting and glass restoration since 1996 remains on sick leave between 2009 and 2010 for 12 months due to asthenia which limited his activities.
During that year he was studied in the Internal Medicine Department of a Tertiary Hospital in relation to asthenia.
A benign thyroid lesion was detected and a total thyroidectomy was performed in May 2010.
After the intervention asthenia persists, which is related to postoperative hypothyroidism, with normal exploratory and analytical findings.
Previously, in January 2010 a blood lead determination was requested for the first time in his laboratory tests, following a casual conversation with his doctor about his work activity.
Lead was detected in 12.8 (range 0.1-10).
Chronic lead poisoning is diagnosed, and protocolized treatment is prescribed, in addition to recommend avoiding contact with lead.
This blood lead level was determined in the 8th month of sick leave, for which reason she had been suffering toxic colitis for 8 months.
In May 2010 (after 13 months of absence of exposure) the blood lead was normal (8.1) In June 2010 is studied in the Hospital Clínico de Madrid for respiratory symptoms consisting of dyspnea on moderate exertion, cough from coughing.
In this study, occupational pneumoconiosis was ruled out.
In September 2010, she resumed her work activity, and a few days later she began with headache, nausea, vomiting, diarrhea/constipation and abdominal colic pain, as well as polyarthralgia and asthenia.
In October 2010 (one month after reincorporation) a new analytical test was performed, in which a blood lead level of 71.2 was detected.
In November 2010, the blood lead level was 59.1.
It is indicated then interruption of exposure to lead, which causes work leave by his Mutue of Work Accidents and Occupational Diseases of Social Security on 11/15/2010, with a plumbemia date of 52/2010.
In December 2010 it was determined that the patient has occupational exposure to lead, with a chronic exposure to which acute exposure overlaps, with probable cardiovascular, renal and osteoarticular involvement (intestinal deposits in april 2010).
Absolute transfer of exposure is indicated.
The patient remains under treatment and should follow the recommendations of the Nephrology Department.
She is referred for control by her Primary Care physician, who currently coordinates specialized care (in charge of Internal Medicine and Nephrology).
As a personal history, she presented acute renal colic in 2004, gout crisis in 2005, bronchitis, depression in 2007 and pneumonia in 2008.
Regarding chronic symptoms, the patient suffered headaches, nausea, vomiting, alternating episodes of diarrhea with constipation, abdominal colic pain, polyarthralgia, nocturia, depression, severe asthenia, dyspnea.
The worker goes to the Medical Consultation of Social Security referring to the symptoms mentioned above, as well as loss of hearing for several years, and provides reports that work in his power.
An evaluation was requested by the otorhinolaryngology consultation of the institution to complete the case.
The results of this audiometry conclude symmetrical sensorineural hearing loss, with UMC in both ears at 70 dB.
Verbal audiometry shows discrimination of 100% to 75-85 dB.
Romberg negative, Rinne positive bilateral.
The patient reported in the consultation of the disability assessment unit of the INSS that in her work there has been no medical-occupational or initial or periodic recognitions due to exposure to toxic substances.
It also presents documentation relating to proposals for corrective measures issued by the licensing service in 2002 at the worker's request.
It also provides a new assessment by the same Service in 2010, reflecting that these remedial measures have not been applied.
These focused mainly on two relevant aspects of the work environment, which were the absence of localized air extraction and the absence of clothing with different cabinets for work and street clothes, as well as showers.
Finally, the Disability Assessment Team of the National Institute of Social Security, gathered to assess the case resolved Total Permanent Disability due to occupational disease for jobs in which there is exposure to lead and other noises fluid exposure.
1.
Case presentation
Limit values and concepts related to lead exposure
According to the lead-specific health surveillance protocol of the Ministry of Health, workers are considered exposed to those who for more than 30 days a year have an environmental concentration > 40 mg/m3 of air per week or > 40 mg/m3 of lead per week for men.
Action levels for lead (those from which biological surveillance of workers should be adopted) are considered an environmental concentration of 75 mg/m3, referring to 8 hours daily and 40 ml/100 ml or a plumbemia weekly.
Limitation periods are those that should not be exceeded and workers should be removed from exposure if they are exceeded.
Lead is 150 mg/m3 of air referred to 8 hours daily and 40 weekly or blood lead levels over 70 ug/100 ml2, 3.
In the list of activities with lead exposure, within the high risk subgroup are, among others, welding of objects and lead alloys, and the manufacture and use of composite paints, enamels and barnic oxides3.
Lead dynamics in the body
The most important route of penetration is respiratory, and its degree of absorption depends on the environmental concentration, exposure time and the physical and chemical form of the product, as well as the working conditions and intrinsic factors of the worker.
More than 50% of the aspirated lead passes into blood after 50 hours of exposure.
The second major route of absorption is oral.
Between 5 and 10% of the lead ingested passes into blood, the rest being eliminated in the faeces.
Finally, the skin pathway is very weak in the case of lead.
Lead elimination is mainly urinary.
Fecal transmission eliminates 80% of the lead ingested plus a small part of the absorbed lead that is eliminated by the bile.
Other routes are saliva, sweat, or milk3.
Platelet in the body
In hematopoietic tissue, lead alters the maturation of red blood cells by inhibiting the synthesis of Hem group in erythroblasts.
In this way, megaloblasts and polyploid erythroblasts are generated, presenting basophilic punctate, which is characteristic of this poisoning.
Additionally, RNA is produced in mature ways.
Regarding blood, a saturnin anemia appears, which is hemolytic and affects me with larger, more fragile red blood cells and reduced half-life4.
In the nervous system, lead interferes with the metabolism of acetylcholine, slowing down the nerve impulse.
This fact appears with blood lead levels above 60 ug/100 ml4.
The involvement of the renal system is progressive.
In the first phase, intranuclear inclusions of lead appear in tubular cells, without affecting renal function.
Interstitial fibrosis follows, and functional involvement begins.
Finally, there is a chronic nephritis with irreversible tubular and glomerular injury2, 4.
Regarding reproduction, lead increases perinatal morbidity and mortality, hypospermia and spontaneous abortion rate.
Lead passes the blood-placental barrier to equalize blood lead levels on both sides.
In bone tissue, calcium displaces from bones to deposit them, increasing bone fragility.
Lead causes hypertension and increases cardiovascular risk due to renal involvement and increased vascular resistance.
Furthermore, cardiac conductive tissue can produce cardiac rhythm alterations.
Clinical
Acute lead poisoning (infrequently nowadays) is associated with significant abdominal pain, vomiting, constipation, seizures and coma that can lead to death, delirium, psychotic episodes, oliguria and cytolysis.
The chronic intoxication, more frequent at present, differentiates three phases.
In the first phase of impregnation, with lower blood lead levels 70ug/100 ml, there are signs of impasse, nervous tissue constipation, malaise, mood changes, fatigue, arthromyalgia, insomnia, decreased blood pressure.
In the following phase, of frank intoxication, saturnine colic, motor polyneuritis that most affect the more active muscles, symmetrical sensorineural hearing loss, saturnin encephalopathy (transient dyschromatic aphasia, transient hypospermia, capturing, hypospermia,
Finally, the terminal phase of chronic intoxication presents permanent hypertension and nephritis associated with gout and cardiac rhythm alterations, in addition to the symptoms and signs of the previous phase2,3,4.
Treatment
Treatment consists of removing the lead source and administering calcium supplements at doses to prevent osteoporosis.
In addition, in cases of elevated blood lead levels (60 ug/100 ml) or severe clinical involvement, chelation is indicated.
Currently, dimercaptosuccinic acid (DMSA) is recommended as chelator, since it has few adverse effects and does not manifest lead to the brain.
Other options are disodium edetate calcium channel blockers (EDTA Ca), and its association with dimercaprol in cases of encephalopathy2,3,4.
1.
Corresponding address: Pablo Honorio Labanda Urbano Hospital de La Princesa.
Occupational Risks.
Area 2.
Diego de León, 62 28006 Madrid.
Spain.
Telephone: (+34) 630831436 E-mail: pablohlabanda@gmail.com
