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Environmental Exposure to Iron, Manganese, and Pecticides: A possible cause of Parkinson's disease

Environmental Exposure to Iron, Manganese, and Pesticides: A possible cause of Parkinson's Disease


Parkinson's disease has been linked to many environmental causes such as pesticides, iron, and manganese (Mn); Parkinson's disease (PD) affects millions of people across the United States. The causation of this disease could be linked to iron and manganese. Many studies look at exposure factors such as the chemical dieldrin. People who live in rural areas are more susceptible to the risk of PD; this could occur through the drinking of contaminated water or extensive exposure to pesticides. The study of welding and the hazards of the fumes that are produced; could pose a link to PD.


Parkinson's disease (PD) causes are unknown, but there are suggestions that contributing factors maybe due to pesticide contamination and chemical contamination such as manganese or iron. The role of the environment show's that people who live in rural areas are more susceptible to the risk of PD through drinking contaminated well water that contain pesticides (Gorrell, DiMonte, and Graham, 1998). Millions of people are affected by PD across the United States; it's a disease that ca n rob an individual of their mobility. Most people are unaware what Parkinson's disease really is and the origins of the disease.

Statement of Problem

Toxins have been known to cause serious environmental problems and health problems. The use of pesticides has had a major impact on the health of many people across the United States. Other chemicals that are linked to PD are iron and paraquat and exposure of these chemicals are considered environmental risk factors (Peng, Peng, Stevenson, Doctrow, and Anderson, 2007, p 6914).

Significance of the Problem

In many studies it has been determined that fumes from welding rods which is known to contain the following elements:  Manganese (Mn), Zinc (Zn), Lead(Pb), Arsenic(As), Calcium(Ca), Sulfur(S), Chromium(Cr), Fluoride(F), and Hafnium(HF) (Racette, Minnich, Moerlein, Mink, Videen, and Perlmutter, 2001 p 8). Other elements such as aluminum, copper, and iron are linked to PD (Rajput 2001, p 4). The average age for the onset of PD is 55 and 5% of those are diagnosed with the disease before the age of 55 years.

Literature Review

Pesticides, Manganese, and Iron

In California; farmers use more than 250 million pounds of pesticides(Yesavage, Sheikh, Neda, Murphy, O'Hara Hierhelzer 2006 et al., p 32). This study determined whether wind blown from contaminated areas of pesticides sites were contributors to the high incidence of PD in various California communities. In this study a clear correlation between PD and pesticides (Yesavage et al., p 34). There were other areas that were contributing factors to PD; such as Mn.

Manganese and Iron

Manganese is a dietary element that is a recommended nutritional intake of 2 to 5 mg/day (Jankevic 2005, p 2022). In a study of 250 patients that already had contracted PD; it was determined that out of 388 individuals in the control group; the higher the iron intake in conjunction with Mn would increase the risk of PD (Jankevic 2004). One of the elements that was found in an autopsy of a patient were the use of excessive amounts of iron located in the substantia nigra (SN) that would be associated with PD (Peng, Peng, Stevenson, Doctrow, and Anderson 2007, p 6914). Another issue is people living in areas that were known for having well water as a means of drinking water; had a high potential of exposure to PD causing contamination (Peng 2007, et al., p 6914).


Pesticide chemicals that were found in autopsied brains were at an elevated amount of organochlorine pesticide dieldrin (Richardson, Candle, Wang, Dean, Pennell, and Miller 2006, p 976). The chemical dieldrin; is no longer used but traces of this chemical is still present; dieldrin has been found in breast milk of 1,436 women living in America (Richardson 2006 et al., p 976). There is evidence that exposure to PD begins at an early age; maybe at the beginning of life at the neonatal stage.

Environmental factors of dopamine transporters (DAT) and vesicular monoamine transports 2 (VMAT2) may increase the susceptibility of dopamine neuronal in degeneration of PD (Richarson et al., p 983). Pesticides use among Californian was very high; 250 million pounds of pesticides were used annually (Ritz and Yu 2000, p 323). In California; 10,000 workers applied agricultural products which required a monitoring of their blood cholinesterase levels; due to excessive exposure. The assessment of exposure was done by counties by way of countywide per square mile by the usage of restricted pesticides in daily farming activities (Ritz and Yu 2000, p 324). Ritz and Yu 2000, p 324, classified 15 counties as high; 9 counties as moderate, and 7 counties as low; and 14 other counties as none or minimal users of agricultural pesticides.
A logistic regression analyst was used for this study with an odds ratio (OR) of 95% confidence interval (CI) for a crude adjustment. Death rates using PD as the cause of death was were 19% to 47% higher in counties that used restricted pesticides (Ritz and Yu, p 325). Adjusting for race, gender, place of birth, age, and education; for people living in counties for more than 40 years who died from PD from 1989-1994; and the prevalence of odds ratios (POR) for various restricted-pesticide use counties and those of counties that never used pesticides; there were 1.52, (95% CI: 1.35-1.72), 1.49 (95%CI: 1.31-1.69), and 1.49 (95%CI: 1.30-1.71) (Table 2) (Ritz and Yu, p 326).

Table 2 Prevalence odds ratios (POR) and (95% confidence interval (CI) for Parkinson's
disease as the underlying cause of death (ICD - 9.332) compared to ischemic heart disease
deaths (ICD-9 410-414) in California by county pesticide use; 1984-1994.
                           1989-                                                                     1984-                       
                                            POR                                                  POR                              

Risk     No. of          Crude             Adjusted          No. of      Crude       Adjusted
Factor   Cases           (95% CI)        (95% CI)         Cases      (95% a >) (95% CI)
No                      137              1.00                    1.00      981    1.0                 1.0
No                      133              1.55                       0        870       0                    0

moderate          1137                1.56
                                                 1.44                                         1.40              1.37                    
high                    703                1.42                 1.45       403    123              1.19 

1.59)             (1.09-1.38)          (1.06-1.34)

Total N
cases                  4533                                                      2983
controls          259,99                                                  238,462
 Adjusted for: age, gender, race (White, Black, Asian, and other), birthplace; California, year
of death, education (^12, 13-15,>15 years). Adjusted for: age, gender, and race(White, Black,
Asian, and otherO, birthplace California, year of death.
Used by peremission from Ritz, B. and Yu, F. (2000)
Parkinson's disease mortality and pesticide exposure in California 1984-1994
International Journal of Epidemiology 29 (2) p 326, Retrieved on May 15, 2008 from

As part of this study logistical regression was used along with a proportional odd mortality studies which was used as an estimate for odds ratio (OR) and a 95% CI for pesticide use as an adjusted rate related to PD (Ritz and Yu, p 325). Also noted is the higher the education the more susceptible those individuals were in contracting PD. The prevalence of OR with a 95% CI for PD; there were 703 reported cases with a 95% CI 1.42 adjusted to (1.45) in 1989-1994. The California study found an increase level of PD in counties that used pesticides. The may be a possible chemical link to Parkinson's disease. The possibility as previously stated of manganese being a link to PD  could be a valid one.

2000; from the Movement Disorders Center located at Washington University School of Medicine in St. Louis, MO (Racette, Minnich, Moerlein, Mink, Videen, and Perlmutter 2001, p 9). The welders in this study reported how many hous they worked daily, how many years they worked, how much exposure to welding before the onset of Parkinsonism symptoms (Racette 2001 et al., p 9). As the study of welders progressed; a control group of 100 patients were used; who were similar in nature to the 15 welders. The second group that was chosen for this study had PD; six patients that had similar characteristic such as age and sex (Racette et al.) and whether are not they had Parkinson's disease. The two-tailed test, unpaired student's t-test was used to compare age at onset and how long did the group have PD. The chi-square analysis was used to determine the frequency of the control group and welders as stated by Racette et al. p 9).

When a comparison was done of the 15 welders against a control group it was determined that idiopathic PD; there wasn't a great difference except for the age difference, (i.e., the control group had a much younger age) at the beginning stages of PD. Upon further study Racette et al., p 12; believed that the exposure to fumes from welding may act as a precursor to PD and other chemical elements that comprise the fumes may also be the cause of PD.

Parkinson's disease

Parkinson's disease is a neurodegenerative disease where the dopaminergic neurons; substantia nigra pars compacta (SNpc) (Peng 2007, p 6914). In 1817 a British physician by the name of James Parkinson; notice people that had problems walking, talking, and just performing daily activities; which lead him to study the behavior of individuals with this disorder (Parkinson, 2007).


Individuals with PD usually end up being administered various types of medication to control various symptoms. It is very important to individuals administering treatment to PD patient that they keep abreast of the different types of medications and the possibility of drug interactions (Parkinson's Disease Foundation, Inc, 2008) (PDFI). Some of the medications that are used for treatment are: Carbidopa/Levodopa, Dopamine agonists, Anticholinergics, and MAO-B inhibitors see Table 3 - Table 8 (PDFI). The drug carbidopa/levodopa (Sinemet©, 2008) substance when used; converts into dopamine by an enzyme in the brain (PDFI). The drug levodopa is the most well known drug in existence today for Parkinson's disease. In the tables that follow are variables of treatment; depending on symptoms and presentation (PDFI, 2008).

Table 3
 Available Doses
 Initial Dosing
 Side Effects

 10/100 mg
25/100 mg
50/200 mg
25/100 mg
2-3 X/day
 Low blood pressure (BP)
nausea, confusion, dyskinesia, dry mouth, dizziness
 First course of treatment
converts to dopamine to
manage major symptoms
Antacids, anti-seizure drugs, anti-depressants, high protein food
 Carbidopa/Levodopa controlled release
(Sinemet CR©)

 10/100 mg
50/200 mg

50/200 mg

 Low blood pressure(BP), nausea, confusion, dyskinesia, dry mouth, dizziness
 First course of treatment converts to dopamine to manage major symptoms and may prolong effectiveness
 Antacids, ant-seizure drugs, anti-depressants, high protein food

Orally disintegrating tablet



Low BP, nausea, confusion, dyskinesia, dry mouth, dizziness

First course of treatment; converts to dopamine to manage major symptoms; also for patients with swallowing difficulties

Antacids, anti-seizure drugs, anti-hypertensives, anti-depressants, high protein food

Stalevo© (carbidopa, levodopa and entacapone) is a combination tablet for patients who experience end-of-dose "wearing off." The tablet combines carbidopa/levodopa with entacapone. While carbidopa reduces the side effects of levodopa, entacapone extends the time levodopa is active in the  (up to 10 percent longer). The same drugs that interact with carbidopa/levodopa and entacapone interact with Stalevo©. Used by permission from Parkinson's Disease Foundation, Inc. Retrieved on May 18, 2008 from  

Table 4
Dopamine agonists are drugs that stimulate the parts of the human brain that receive dopamine. In effect, the brain "thinks" it is receiving dopamine, so these drugs help satisfy the brain's need for dopamine. Dopamine agonists can be taken alone or in combination with medications containing lebvodopa.  Agonists available in the United States include bromocriptine (Parlodel©). In March 2007, the dopamine agonist pergolide (Permax) was pulled from the manufacturer of Neupro© (rotigotine transdermal system), recalled the drug because of concern of a deviation from approve product standards that has apparently reduced the effectiveness of the treatment. Consultt a doctor before taking any of the following to avoid possible interactions: alcohol, anti-psychotics, medications that lower blood pressure, Navane© (thiothixene), Taractan© (chlorprothixene), Haldol© (haloperidol), Reglan© (metoclopramide), phenothiazines, thiozanthenes, cimetidine, phenothiazines, butyrophenones, Cipro© and benzodiazepines.      
Side Effects
.02 mL-.06 mL

.02 mL during "off" periods
Nausea, vomiting, low, sleepiness, dyskinesias, hallucinations, chest pain 
Adjunct levodopa therapy to treat "off"periods
5HT3 agonist (for example, Zofran©,
and Zestril©
2.5 mg
5 mg
2.5 mg3X/day
Low BP, nausea, edema, confusion, dry mouth, depression, headaches
First course of treatment alone or with  levodopa; mimics dopamine to manage major symptom
Alcohol, anti-psychotics, blood
pressure lowering medications
One 2 mg patch a day
Nausea, application site reactions, somnolence, dizziness, headache, vomiting, sleep attacks, insomnia
First course of treatment alone or with levodopa in early-stage idiopathic Parkinson's disease; mimics dopamine to manage major symptoms
May cause allergic-type reactions including anaphylactic symptoms expecially in people sensitive to sulfites, including those with asthma.
.125 mg
.25 mg
.5 mg
1 mg
1.5 mg
.125mg 3X/day
Arthritis, chest pain, nausea, low BP, sleep disturbances, sedation
First course of treatment alone or with levodopa; mimics dopamine to manage major symptoms
Sedatives and tranquilizers; metocipramide, thiozanthenes, cimetidine, phenothiazines, butyrophenones
.25 mg
.5 mg
1 mg
2 mg
3 mg
4 mg
5 mg
.25 mg2X/day
Abdominal pain, sleep disturbances, nausea, low BP
First course of treatment alone or with levodopa; mimics dopamine to manage major symptoms
  Alcohol, anti-depressants,
Cipro©, anti-psychotics, benzodiazipines
  Used by permission from Parkinson's Disease Foundation, Inc. Retrieved on May 18,2008 from

Table 5

    Anticholinergics(trihexphenidyl, benziropine mesylate, procyclidine, etc) do not act directly on the dopaminergic
    system. Instead they decrease the activity of another neurotransmitter that controls movement; called acetylcholine, to
    balance out the production of dopamine and acetylcholine. In general, mild PD that consists of tremor at rest can often
    be treated initially with anticholinergic agents.  Adverse effects of these drugs include blurred vision, dry mouth and
    urinary retention. Anticholinergics may be contraindicated in older patients because they can cause confusion and        
    Haldol©, Thorazine©, Symmetrel©, Cllozaril©, and alcohol

Available Doses
Initial Dosing
Side Effects
.5 mg
.5 mg2X/day
Confusion, halluncinations, nausea, blurred vision, dry mouth, urinary retention, nervousness; not used long-term due to side effects
Secondary medication; tremor; attempts to restore balance by inhibiting other enzymes and nerve cells that may attack dopamine
  Anti-histamines, Propulside©,
Symmetrel©, Clozaril©,
 1 mg
 2 mg
 1-2 mg 2X/day
 Confusion, hallucinations, nausea, blurred vision, dry mouth, urinary retention, nervousness; not used long-term due to side effects
 Secondary medication; tremor; attempts to restore balance by inhibiting other enzymes and nerve cells that may attack dopamine
    Used by permission from Parkinson's Disease, Inc. Retrieved on May 18, 2008

Table 6

MAO-B inhibitors© such as selegiline or deprenyl (Eldpryl©) are used to block an enzyme in the brain that breaks down levodopa. They have been shown to delay the need for Sinemet© when prescribed in the earliest stage of Parkinson's, and have also been approved for use in later stages of the disease to boost the effects of Sinemet©. Elderpryl© may interact with anti-depressants, narcotic pain killers and decongestants. Check with a doctor before taking any new medications.    

Available Doses
Initial Dosing
Side Effects
5 mg
5 mg 2X/day
(max dose)
Agitation, insomnia, hallucinations
Tertiary medication; controls brain's metabolism of dopamine
Anti-depressants, narcotic painkillers, decongestants

Selegiline HCL
1.25 mg
1.25 mg
Dizziness, nausea, pain, headache, insomnia, rhititis, dyskinesias, back pain, stomatitis, dyspepsia
Adjunct to levodopa in patients with significant "off" peeriods
Anti-depressants, narcotic painkillers, decongestants  

 0.5 mg
1 mg
 0.5 mg 1X/day
 Increased dyskinesias, postural hypotension, headaches, joint pain, indigestion
 Signs and symptoms of PD as initial monotherapy and adjunct to levodopa
 High tyramine content foods (for example, draft beer, red wine, aged cheeses, soy sauce and other products), narcotic painkillers, anti-depressants, decongestants
    Used by permission from Parkinson's Disease Foundation, Inc. Retrieved on May 18, 2008 from:

Table 7

COMT Inhibitors© such as entacapone (Comtan©) represent a different class of Parkinson's medications and they must be taken with levodopa. COMT inhibitors prolong symptom relief by blocking the action of an enzymne which breaks down levodopa, allowing a larger amount of levodopa to reach the brain, which raises the dopamine level. This helps provide a more stable, constant supply of levodopa. 

Available Doses
Initial Dosing
Side Effects
200 mg

200 mg with
levodopa; max 8 per day

Abdominal pain, back pain, constipation, nausea, diarrhea, blood in urine
Secondary medication; delays wearing off by prolonging effectiveness of levodopa
  MAO inhibitors

100 mg
200 mg
 100 mg 3X/day

Abdominal pain, back pain, constipation, nausea, diarrhea, blood in urine, liver failure
 Tertiary medication for motor fluctuations; limited in use to those who have exhausted other treatment options
MAO inhibitors

Table 8

Other medications

     Used by permission from Parkinson's Disease Foundation, Inc. Retrieved on May 18, 2008 from:

Material Safety Data Sheet

The material safety data sheet (MSDS) was introduced for workers and emergency personnel to assist in the proper procedural method in handling and working with different hazardous substances (MSDS, 2008). The material safety data sheet is for employees whom work around or with hazardous material and for the use of emergency responders in the event of an emergency and a need to know what chemicals were involved. Manganese is chemical substance that's been considered as a cause of PD. Manganese (Mn) poisoning from welding; many physicians are unaware of these findings and what is stated in a MSDS. The following are synmptoms of Mn poisoning:
     1. There may be tremors, shakes , loss of balance, slowed movement, walking problems, impotency, slurred speech, extreme drowsiness or nighttime leg cramps (International Brotherhood of Electrical Workers, 2003) (IBEW).
The above symptoms may be similar in nature for many welders and is probably mistaken for Parkinson's disease, Lou Gehrig's disease (ALS) or Multiple sclerosis (MS) (IBEW).
The Occupational Safety and Health Administration (OSHA) created by the Occupatyional Safety and Health Act of 1970 (Centers for Disease Control and Prevention, 2008 (CDC)).

Occupational Safety and Health Act of 1970

The National Institute for Occupational Safety and Health (NIOSH) and the Occupational Safety and Health Administration (OSHA) were both created by the Occupational Safety and Health Act of 1970 (CDC, 2008).

Conclusion and Recommendation

Pesticides do show a linkage of contracting PD and the chemical exposure to pesticides. Individuals that mixed or applied pesticides; there was a positive association in the amount of incident of PD (Kamel et al., p 368). Parkinson's disease will be on the rise in the United States by an estimated increase of 1.3 million people by the year 2040 (Muir and Zearac 2001, p 888). The House Appropriations Committee would like for the National Institute of Environmental Health Sciences (NIEHS) to continue funding research into Parkinson's disease environmental influences (NIEHS, 2007). The NIEHS continue to make Parkinson's disease and other neurodegenerative diseases there priority in which $2 million dollars is available under program announcement, PAS 03-160, "Gene-Environmental Interactions in Neurodegenerative Disease," and the national network of the Collabortive Centers for Parkinson's Disease Environmental Reasearch (CCPDER) (NIEHS). Through the continued support of NIEHS in the study of Parkingson's disease and the collaboration with (CCPDER) to facilitate data sharing with other epidemiologist and improvement of identifying environmental toxicants will assist in as better collaborative effort (NIEHS, 2007).


Centers for Disease Control and Prevention (2008) NIOSH origins and mission National Occupational Safety and  Health   
          Retrieved on May 24, 2008 from
Kamel, F., Tanner, C.M., Umbach, D.M., Hoppin, J.A., Alavanja, M.C., et al. (2006)
          Pesticide exposure and self-reported Parkinson's disease in the agricultural health study
          Am Journal of Epidemiology 165(4) pp 364-374, p 368 Retrieved on March 5, 2008 from
Gorrell, J.M., DiMonte, D., and Graham, D. (1996) The role of the environment in Parkinson's disease
          Environmental Health Perspective 104(6) pp 1-4 Retrieved on March 30, 2008 from
International Brotherhood of Electrical Workers (2003 July/August) Welding and manganese poisoning
          IBEW Journal Retrieved on May 24, 2008 from

Jankovic, J. (2005) Searching for a relationship between manganese and wilding and Parkinson's disease Neurology
          64 p 2022, 2024 Retrieved on March 30, 2008 from
Muir, T. and Zegarac, M. (2001) Societal costs of exposeure to toxic substances: economic and health costs of four
           case studies that are candidates for environmental causation Environmental Health Perspectives
           109(6) p 888 Retrieved on March 10, 2008 from 
MSDS(2008) The msds faq Retrieved on May 25, 2008 from
National Institute of Environmental Health Science (2007) Significant items in house & senate appropriations
           committee reports: fy 2006 house appropriations committee report language, house report 109-143
           Retrieved on May 24, 2008 from
Parkinson, J (n.d.) Web Parkinson's disease-not-for-profit organization Retrieved on May 14, 2008

Peng, J., Peng, L., Stevenson, F.F., Doctrow, S.R., and Anderson, T.K. (2007) Iron and paraquat as synergistic
           environmental risk factors in sporadic Parkinson's disease accelerate age-related neurodegeneration
           The Journal of Neuroscience 27(26) 6914-6922 Retrieved on March 17, 2008 from
Racette, B.A., Minnich, L., Moerlein, S.M., Mink, J.W., Videen, T.O. and Perlmutter, J.S. (2001)
           Welding-related Parkinsonism: clinical features, treatment, and pathophysiology Neurology 56 p 8, 9, 12
            Retrieved on March 30, 2008 from http://www.neurology.,org/cgi/reprint/56/1/8
Rajput, A.H. (20-01) Environmental toxins accelerate Parkinson's disease onset Ameerican Academy of Neurology
            56 p 4-5 Retrieved on March 30, 2008 from
Richardson, J.R., Caudle, W.M., Wang, M., Dean, E.D., Pennell, K.D. and Miller, G.W. (2006)  Developmental
            exposure to the pesticide dieldrin alters the dopamine systems and increases neurotoxicity in an animal
            model of Parkinson's disease The FASEB Journal 20(10) p E976, E983 Retrieved on March 30, 2008
Ritz, B. and Yu, F. (2000) Parkinson's disease mortality and pesticide exposure in California 1984-1994
            International Journal of Epidemiology 29 p 323-326 Retrieved on March 30, 2008 from
Sinemet© (2008) Indication and dosage Merck & Company, Inc. Retrieved on May 24, 2008 from
Yesavage, J.A.,Sheikh, J., Noda, A., Murphy, G., O'Hara, R., Hierholzer, R. et al. (2006) Spatial test for agricultural
            pesticide "blow-in" effect on prevalence of parkingson's disease Journal of Geriatric Psychiatry and Neurology
            19 pp 32-34 Retrieved on March 5, 2008 from










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